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CLINICAL  DISORDERS 
OF  THE  HEART  BEAT 

A  Handhoo\for  Practitioners  (f^  Students 

BY 

Thomas  Lewis,  M.D.,  F.R.S.,  D.Sc,  F.R.C.P. 

Physician  of  the  Staff  of  the  Medical  Research  Commiitee;  Assistant  Physician  and 

Lecturer  in  Cardiac  Pathology,  University  College  Hospital;  Late  Physician  to 

Out  Patients,  City  of  London  Hospital  for  Diseases  of  the  Chest. 


[fifth  edition] 


NEW  YORK 

PAUL  B.  HOEBER 
1 92  I 


1'     ■    a> 


^  « 


By:  the  same  Author: 
J  I 
The  MECHANfsM  and  Graphic 

Registra'Hon  of  the  Heart  Beat 

With  Especial-fkeference  to  its  Clinical  Pathology 
/  $16.00  ntl 

Clinical  jSisorders  of  the  Heart  Beat 

Fifth  EditioiT,  $3.00  net 

Clinical  Jlectrocardiography 

^tcond  Edition,  $3.00  net 

The  SolArs  Heart  and  the  Effort 

SyNDrSiE  $2.50  net 

Lectures%n  the  Heart  $2.50  net 

Heart 

A  Journal  for  the  Study  of  the  Circulation 
Edited  b)i  Thomas  Lewis.       Per  Volume,  $7.50  net 

PAUL  B.  HOEBER,  Publisher 
67'69  East  ^qth  Street,  New  York 


f 

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\ 


V  ♦ 


.# 


PREFACE.    \ 


DURIN0  recent  year's  our  IjrS^leclgeTof  the  heart 
and  of  its  affections  h^^^xapidly  advanced. 
The  newly  acquired  knowledgexiaae  ibieen  gathered 
largely  by  precise  graphic  methodM-.^.^b  th^  onlooker 
it  often  appears  that  this  ^dvancej  simply:;;\^omprises 
a  detailed  analysis  and  iaccurat^*  classifica^^'^m.  of 
cardiac  irregularities.  ThatXis  awuite  inadequate 
review  ;  recent  study  has  done  mux^  more  for  us  than 
that ;  it  has  thrown  most  of  the  major  conceptions 
of  heart  disease  into  a  melting  pot,  from  which  some 
have  issued  transformed,  from  which  others  will  never 
emerge.  The  conceptions  of  heart  failure,  gradual  or 
sudden,  and  of  the  role  which  valvular  defects,  and 
strain  in  the  wider  sense,  play  in  its  production,  have 
undergone  radical  revision.  The  chief  symptoms  of 
heart  disease,  breathlessness,  exhaustion,  pain,  s^aicope, 


iv.  Preface. 

palpitation,  and  tlieir  relations  to  other  phenomena  of 
heart  disease  begin  to  be  understood  ;  so  do  a  liost 
of  pli3^sieal  signs  which  formerly  were  quite  obscure. 
The  basis  of  prognosis  and  of  treatment  has  been 
profoundly  altered.  Much  of  the  cardiological  work 
and  teaching  of  the  last  century  rested  upon  traditional 
doctrines  which  we  now  recognise  to  liave  been 
unsound.  The  methods  employed  ^^'ere  almost  Avholly 
subjective,  and  consequently^  open  to  very  serious 
fallacies.  Objective  methods,  and  the  graphic  metliod 
in  particular,  have  reformed  our  conceptions. 

Familiarity  with  the  heart's  mechanism  in  health 
and  disease  is  a  first  essential  if  these  newer  concep- 
tions are  to  be  appreciated.  Judged  by  present-day 
standards,  tliose  who  do  not  possess  this  familiarity 
are  not  competent  to  deal  witli  cardiac  patients.  I 
make  this  statement  after  full  consideration,  speaking 
of  cardiac  patients  generally,  and  without  confining 
it  to  patients  who  exhibit  irregular  action  of  the  heart. 
Confirmed  in  this  view,  I  am  asked  again  after  eight 


Preface.  v. 

years — for  it  is  now  eight  ^^ears  since  the  first  edition 
of  this  book  was  written — ^in  what  degree  is  an 
acquaintanceship  with  graphic  method  essential  or 
expedient  in  the  routine  of  busy  practice  ?  To  this 
I  reply,  as  I  replied  then,  that  the  acquisition  of  the 
necessary  manipulative  skill  and  experience,  which  the 
taking  and  interpreting  of  graphic  records  involves, 
will  often  entail  too  great  an  expenditure  of  time  and 
energy  adequately  to  repay  the  practitioner  or  the 
patient  he  serves.  A  universal  and  detailed  acquaint- 
anceship with  medical  science  as  it  exists  to-day  is  no 
longer  possible,  but  it  behoves  a  practitioner  to  grasp 
new  principles  and  to  be  conversant  with  new  knowledge 
and  its  influence  upon  the  care  of  patients  afflicted 
with  common  maladies. 

While  the  pursuit  of  graphic  work  by  those  who 
possess  the  special  aptitude  or  a  developing  interest 
in  the  method  is  decidedly  to  be  encouraged,  yet 
it  is  clear  that  the  universal  adoption  of  graphic 
method  is  neither  to  be  anticipated  nor  advocated. 


vi.  Preface. 

And  this  conclusion  is  largely  dictated  by  the  belief 
that  most  of  the  every-day  disturbances  of  the  heart 
beat  may  now  be  identified  by  relatively  simple  means. 
If  this  is  possible  to  a  practitioner,  then  it  is  also 
possible  for  him  to  grasp  the  new  general  conceptions 
and  to  apply  them  in  his  dail}'  work. 

More  than  nine  years  ago,  and  at  a,  time  when 
I  was  actively  engaged  in  studying  cardiac  irregularities 
by  exact  graphic  method,  these  thoughts  were  in  my 
mind  ;  they  led  me  to  search  for  a  series  of  relatively 
simple   tests,    based   upon   enquiry    into    the   clinical 
histories  of  patients  and  upon  bedside  methods  then 
general^  in  vogue,  by  which  the  common  disorders 
of   the   heart   beat   might   be  recognised.        For   this 
purpose  I  made  a  large  number  of  observations  and 
incorporated  in  this  handboolv  tlie  ne\\    information 
so  gathered  ^^  ith  that  gained  from  the  contemporary 
writings  of  my  co-workers.     That  its  publication  has 
been  justified  I  judge  from  the  repeated  calls  for  new 
editions.     I    have    again   revised   the   text,    and   still 


Preface.  vii. 

confine  the  graphic  records  ahnost  to  such  as  ilhistrate 
what  ma}^  be  seen  and  felt.  There  are  few  important 
disorders  of  the  heart  beat  which  the  unaided  and 
practised  senses  may  not  recognise.  A  single  and 
portable  piece  of  apparatus  may  be  used  in  cases  of 
doubt  to  supplement  the  observations  so  obtained. 
The  Dudgeon  sphygmograph  is  probably  familiar  to 
most  medical  men  ;  it  will  readily  trace  a  short  curve 
from  the  radial  pulse.  Such  a  curve,  especially  if  it  be 
accompanied  by  a  record  of  time,  will  usually  complete 
an  analysis  of  any  common  disorder  of  the  heart  beat. 
The  purpose  of  this  handbook  is  not  to  discuss 
the  evidence*  upon  which  the  diagnosis  of  cardiac 
disorders  rests,  but  simply  to  recount  such  symptoms 
and  signs  as  I  have  found  to  be  serviceable  in 
identifying  these  disorders,  without  recourse  to  complex 

graphic  methods. 

THOMAS  LEWIS. 

August,   1920. 


*  A  full  account  of  this  evidence  will  be  found  in  my  other  publications. 


(     ix.     ) 


CONTENTS. 


CHAPTER  I. 

Page 
The  identification  of  disoedeks  of  the  heart  beat  .  .  . .  .  .         1 

Preliminary  evidences  .  .  .  .  .  .  .  .  .  .  .  .         4 

Age  ;  heart  rate  ;  2^srsistence  of  irregularity. 

Common  types  of  disorder  and  their  meaning       .  .  .  .  .  .  6 

Solitary  pulse  intermittences ;  coupled  heats ;  triple 
heating  ;  halved  pulse  rate  ;  a  grossly  irregular  pulse ; 
a  mild  grade  of  irregularity. 


CHAPTER  II. 

Sinus  irbegltlaeities         . .          . .          . .          . .          . .  . .  . .  8 

Definition   .  .          .  .          .  .          .  .          .  .          .  .  .  .  .  .  8 

The  nature  of  sinus  disturhances .  .           .  .           .  .  .  .  .  .  8 

Respiratory  irregularities  .  .          .  .          .  .          .  .  .  .  .  .  12 

Sinus  irregularities  which  bear  no  relation  to  respiration  .  .  14 

The  recognition  of  sinus  irregularities     .  .           .  .  . .  .  .  15 

The  jyrognostic  significance  of  sinus  irregularities  ..  ..  16 


X. 


Contents. 


CHAPTER  III. 

Heart-block 

Definition  . . 

The  iMture  of  Jieart-block  . . 

Etiological  and  pathological  relations 

Age  and  sex  ;  heredity  ;  relations  to  infective  diseases  ; 
relation  to  chronic  degenerative  jjrocesses  of  more  obscure 
origin  ;  heart-block  as  a  result  of  digitalis  administration  ; 
special  morbid  anatomy. 

The  recognition  of  heart-block 

Effects  on  the  circulation  and  the  general  symptomatology 

The  progyiosis 

Tlie  treatment 


Page 
17 

17 

17 
21 


25 

32 
36 

38 


CHAPTER  IV. 


Pbematuiie  contractions  or  extrasystoles   . . 

Definition  . . 

The  nature  of  premature  contractions 

Etiological  and  pathological  relations 

Age,  and  sex  ;  associated  conditions  and  provocative  factors 

The.  recognition  of  premature  contractions 

The     subjective     phenomena     which     accompany     premature 
contractions     . .      ■    . . 

The  prognosis  and  treatment 


41 
41 
41 
44 

47 

53 
54 


Contents. 


XI. 


CHAPTER  V. 

Simple  PAuoxYSMAi  tachycardia 

Definition  . . 

The  nature  of  simple  paroxysmal  tachycardia    .  . 

Etiological  and  pathological  relations 

Age  and  sex  ;  heredity  ;  relations  to  infective  disease  ; 
associated  conditions ;  factors  promoting  attacks  ;  fnorbid 
anatomy. 

The  recognition  of  simple  paroxysmal  tachycardia 
Symptomatology  of  paroxysmal  tachycardia 
Differential  diagnosis        .... 
The  prognosis 
The  treatment 


Page 
57 

57 

57 

59 


61 
64 
67 
70 
73 


CHAPTER  VI. 

Auricular  flutter 
Definition   .  . 

The  nature  of  auricular  flutter 
Etiological  and  pathological  relations 

Age  and  sex  ;  relations  to  infective  disease,  etc.  ;  associated 
conditions  ;  morbid  anatomy. 

The  recognition  of  flutter  .  . 

During  the  2  :  1  heart-block  phase  ;  during  the  stage  of 
irregular  responses  :  when  the  responses  of  the  ventricle 
are  infrequent. 

The  symptomatology  of  flutter 

The  prognosis 

The  treatment 


76 
76 
76 
79 


79 


83 
86 

87 


xu. 


Contents. 


chaptp:r  VII. 

AURICtTLAE  FIBRILLATION      .  . 

Definition   .  . 

The  nature  oj  auricular  Jibrillalion 

Etiological  and  jiatliological  relations 

Age  and  sex  ;  relation  to  infections,  associated  conditions  ; 

morbid  anatomy. 
The  recognition  of  auricular  fibrillation 

The  general  symptomatology 

Influence  upon  thrombosis  and  infarction 

Remarks  upon  diagnosis  .  . 

The  prognosis 

The  treatment 

Paroxysmal  fibrillation 

Acute  fibrillation  .  . 


Page 
89 


91 


01 

101 

103 

103 

105 

106 

HI 

.   112 

CHAPTER  VIIT. 


Alternation  of  the  heart  ..  ..  ..  ..  ..  ..  113 

Definition   ..  ..  ..  ..  ..  ..  ..  ..  113 

The  mechanism  in  alternation  of  the  heart  .  .  .  .  .  .  113 

Etiological  and  pathological  relations       .  .  .  .  .  .  .  .  114 

The  recognition  of  jiulsus  alternus  ..  ..  ..  ..  116 

The  subjective  sensations  of  patients  presenting  jndsus  cdternans  118 

The  prognosis         .  .  .  .  .  .  .  .  .  .  .  .  .  .  119 

The  treatment         120 

Index  121 


Chapter  I. 

THE    IDENTIFICATION     OF     DISORDERS    OF    THE 
HEART    BEAT. 

It  seems  desirable  that  I  should  open  the  chapters  of 
this  book  by  acquainting  my  readers  with  the  general 
arrangement  of  the  matter  contained  therein. 

Since  those  who  work  amongst  the  sick  usually  become 
interested  in  a  particular  phenomenon  by  observing  it 
rather  than  by  reading  of  it,  I  begin  the  first  chapter  by 
describing  in  general  terms  the  chief  derangements  of  the  rata 
and  sequence  of  the  pulse  and  heart  beat  as  they  are  felt,  seen„ 
or  heard  by  all  practitioners.  I  take  certain  common  and 
generally  recognised  physical  signs  as  they  are  noted  at  the 
bedside  and  translate  these  signs  into  terms  of  mechanism, 
without  attempting  to  describe  the  manner  in  which  they  are 
brought  about  and  without  suggesting  their  value  in  prognosis 
or  treatment.  I  shall  speak  of  seven  forms  of  cardiac  disorder^ 
and  they  will  be  described  under  the  following  headings  : — 

1.  Sinus  arrhythmia. 

2.  Heart-block. 

3.  Premature  contractions  or  extrasy stoles. 

4.  Sirnple  paroxysmal  tachycardia. 

5.  Auricular  flutter. 

Q.  Auricular  fibrillation. 
7.  Alternation  of  the  heart. 


2  Chapter  I. 

There  may  be  some  to  whom  these  terms  are  unfamiliar 
or  to  whom  their  meaning  is  still  obscure.  My  immediate 
endeavour,  therefore,  is  to  offer  them  a  preliminary  idea  of 
the  meaning  of  these  names,  an  idea  which  I  hope  may  appeal 
to  them  from  their  past  experience  ;  and  I  do  so  by  citing- 
clear  examples  of  phenomena  to  which  in  future  I  must 
perforce  refer  in  distinctive  terms. 

If  we  feel  the  pulse  of  a  young  adult,  when  the  breathing 
is  deep,  or,  better  still,  if  we  feel  the  beating  of  a  dog's  heart 
against  the  chest  wall,  a  periodic  irregularity  of  the  pulsa- 
tions is  observed  which  accompanies  the  separate  acts  of 
breathing.  I  cite  this  disorder  of  the  heart  beat  as  a 
characteristic  example  of  sinus  arrhythmia,  or  one  in  which 
the  whole  heart  is  involved. 

In  many  patients  in  whom  the  pulse  and  heart  beats 
fall  ^\ith  perfect  uniformity  for  long  periods,  an  occasional 
and  isolated  disturbance  is  noticed.  The  pulse  intermits  ; 
it  loses  one  of  its  serial  beats  at  intervals.  When  the  heart 
is  examined  it  is  found  that  at  the  moment  of  the  disturbance 
a  ventricular  contraction  appears  before  the  rhythmic,  beat 
is  due,  and  that  this  early  beat  is  followed  by  a  pause  of 
unusual  length.  I  cite  this  disturbance  as  a  simple  example 
of  premature  contraction  or  extrasystole. 

If  in  a  similar  case,  where  the  occasional  j)ulse  fails,  a 
similar  failure  of  ventricular  action  is  discovered,  so  that  on 
listening  at  the  apex  beat  no  abnormal  sounds  are  heard,  but 
the  heart  remains  silent  throughout  the  whole  of  the  pause,  the 
phenomena  are  evidences  of  another  condition,  namely  heart- 
block.  But  lest  I  should  create  confusion  at  an  early  stage,  I 
must  add  that  heart-block  manifests  itself  in  many  other  ways, 
foi  example,  by  j)roducing  pulses  of  conspicuously  slow  rate. 


Disorders  of  the   Cardiac  Mechanism.  3 

Paroxysmal  tachycardia  is  a  term  which  is  probably 
familiar  to  all,  but  I  employ  it  in  a  restricted  sense,  and 
speak  only  of  instances  in  which  an  absolutely  abrupt 
acceleration  of  regular  heart  beat,  which  subsequently 
terminates  in  an  equally  abrupt  manner,  is  repeated  from 
time  to  time. 

Sometimes,  and  especially  in  the  elderly,  we  find  regular 
and  accelerated  heart  action  at  rates  of  120  to  160  per  minute. 
Such  an  acceleration,  when  notable  for  its  constant  rate 
under  all  sorts  of  conditions  and  for  its  tendency  to  persist 
without  apparent  cause,  is  generally  the  result  of  auricular 
flutter. 

When  a  patient,  who  is  known  to  have  mitral  stenosis 
and  who  requires  treatment  for  cardiac  failure,  exhibits  not 
only  dropsy,  venous  engorgement  and  cyanosis,  but  a  rapid 
and  utterly  disordered  heart  action  in  v\^hich  there  is  no 
rhythmic  sequence,  he  presents  a  characteristic  picture 
of  auricular  fibrillation. 

Finally,  if  in  a  case  of  renal  disease  or  arterio-sclerosis 
the  pulse  tension  is  high,  Cheyne-Stokes'  breathing  perhaps 
is  present,  and  the  pulse  is  regular  in  rhythm  but  varies  in 
force,  so  that  each  alternate  beat  is  strong  and  each  alternate 
beat  is  relatively  weak,  an  example  of  alternation  of  the  heart 
is  under  observation. 

I  have  deliberately  chosen  these  examples  because  they 
are  distinctive  ;  but  the  several  forms  of  disturbance  are  not 
always  so  clearly  differentiated.  Were  it  so,  my  task  would 
be  simple.  The  examples  are  distinctive  and  consequently 
allow  a  preliminary  idea  of  my  terms  to  be  entertained. 
It  is  into  these  terms  that  I  shall  in  the  first  instance  translate 
the  commoner  physical  signs,  and  I  do  so  with  the  object 


4  Chapter    I. 

of  providing  the  student  or  practitioner  with  an  immediate 
clue  to  the  type  of  mechanism  with  which  he  is  dealing. 
But  as  this  preliminary  description  is  inadequate,  it  is 
supplemented  by  a  detailed  account  of  each  form  of  disorder 
in  the  remaining  chapters  of  the  book,  in  which  an  account 
of  the  pathology,  prognosis  and  management  will  also  be 
found. 

Preliminary  evidences. 

Am,.  The  first  guide  in  identifying  a  disordered  heart 
mechanism  is  the  age  of  the  patient  in  whom  it  occurs  and  a 
knowledge  of  the  age  incidence  of  the  several  disorders. 

x4.n  irregularity  of  heart  or  pulse  found  before  the  tenth 
year  is  usually  sinus  arrhythmia.  Heart-block  may  be 
present  during  the  first  decade,  but  it  is  rare;  premature 
contractions  have  been  noted  in  c^uite  young  children,  in 
most  of  whom  enlargement  of  the  heart  has  been  present, 
or  during  the  course  of  acute  infections.  Solitary  examples 
of  auricular  fibrillation  have  been  recorded  at  the  ages  of 

5  and  13  ;  it  is  very  rare  before  the  age  of  17. 

The  relative  frequence  of  the  different  disorders  of  the 
heart  beat  from  adolescence  to  old  age  is  in  general  hospital 
practice  approxim.ately  as  follows  : — 

Auricular  fibrillation    .  .          .  .  .  .           .  .  40% 

Premature  contractions              .  .  .  .           .  .  ^5% 

Alternation  of  the  heart            . .  . .          . .  10% 

Paroxysmal    tachycardia,    sinus  arrhythmia, 

heart-block  and  flutter       . .  .  .          . .  15% 

Dealing  Avith  those  in  whom  there  is  obvious  cardiac 
failure,  at  least  60%  of  irregular  hearts  are  irregular  because 
the  auricles  are  fibrillating. 


Disorders  of  the   Cardiac  Mechanism.  5 

Heart  rate.  Another  valuable  clue  is  the  rate  of  the  heart 
beat.  When  the  ventricle"^  heats  regularly  and  its  rate  is 
continually  below  35  beats  per  minute,  complete  heart-block 
is  probably  present  ;  in  similar  circumstances  a  rate  which 
lies  constantly  between  40  and  50  should  arouse  a  suspicion 
of  partial  heart-block  ;  a  persistent  rate  of  130  and  over  in  a 
resting  patient  should  always  suggest  a  long  continued 
paroxysm  of  tachycardia  or  auricular  flutter. 

If,  on  the  other  hand,  the  ventricle  heats  irregularly 
and  its  rate  surpasses  120  per  minute,  fibrillation  of  the 
auricle  is  probably  present,  and  as  the  rate  is  faster,  so  the 
probability  that  such  is  the  disorder  approaches  certainty. 
Irregular  hearts,  beating  at  140  and  over,  are  scarcely  ever 
affected  in  any  other  manner.  Premature  contractions  very 
rarely  accompany  ventricular  rates  of  120  and  over,  sinus 
arrhythmias  are  almost  confined  to  rates  below  100  ;  both 
these  forms  of  irregularity  become  more  frequent  as  the 
scale  of  rate  is  descended  to  the  sixties  and  fifties.  If  an 
irregularity  is  observed,  any  influences,  such  as  exercise, 
fever,  or  the  administration  of  belladonna,  which  enhance  the 
ventricular  rate,  tend  to  abolish  all  irregularities  of  rhythm, 
with  the  exception  of  that  due  to  auricular  fibrillation,  and  in 
this  instance  the  disorder  persists  and  is  usually  augmented. 

Persiste,nceof  irregularity.  Auricular  fibrillation  is  usually 
persistent,  and  examination  from  hour  to  hour  or  from  day 
to  day  reveals  continuous  irregularity.  The  other  irregular- 
ities are  transient,  the  pulse  being  perfectly  regular  from  time 
to  time  ;  shorter  or  longer  periods  of  normal  heart  action 
intervene  between  periods  of  disturbance. 

*  When  I  refer  to  beats  of  the  heart  or  of  the  ventricle,  on  this  or 
future  occasions,  I  do  not  refer  to  pulse  beats.  Ventricular  irregularity  and 
pulse  irregularity  are  not  always  coincident ;  the  ventricular  rate  often 
surpasses  the  pulse  rate. 


6  -  Chapter    I. 

Common  types  of  disorder  and  their  meaning. 

Solitary  pulse  intermittences .  An  occasional  pause  of 
pronounced  length,  which  interrupts  an  otherwise  perfectly 
regular  pause,  is  due  to  one  of  two  causes,*  namely,  a  pre- 
mature contraction  (common),  or  a  dropped  beat  resulting 
from  heart-block  (rare).  They  are  easily  distinguished,  for 
the  premature  beat  is  felt  or  heard  at  the  apex,  it  gives  rise  to 
an  early  first,  or  early  first  and  second  sound.  In  block  the 
heart  is  silent  and  motionless  during  the  whole  pause. 

Coupled  heats.  If  the  ventricular  beats  are  coupled  and 
the  couples  are  evenly  spaced"]*  they  are  the  result  of  one  of 
two  disturbances,  for  either  the  alternate  beats  of  the  normal 
rhythm  have  been  replaced  by  premature  contractions — 
in  which  case  the  second  beat  of  the  couple  is  weak  and  may 
not  reach  the  wrist — or  else  each  third  ventricular  contraction 
has  been  lost  and  heart-block  is  present.  If  the  pulse  beats 
are  coupled  {jndsus  higeminus)  a  third  possibility  remains  ; 
the  pulse  pairing  may  be  due  to  the  occurrence  of  premature 
heart  beats  which  replace  each  third  rhythmic  beat.  If  such 
is  the  case  the  premature  beat  will  be  appreciable  at  the 
apex,  though  it  does  not  reach  the  wrist. 

Triple  heating.  To  recognise  the  cause  we  proceed 
along  similar  lines.  Tripling  at  the  apex  is  due  to  premature 
contractions  which  replace  each  third  rhythmic  beat,  or 
to  heart-block  in  which  each  fourth  ventricular  contraction 
is  lost.  Tripling  at  the  pulse  {pulsus  trigeminus)  may  be 
due  to  a  third  cause,  namely,  premature  beats  replacing  each 
fourth  rhythmic  beat,  the  early  beats  failing  to  reach  the  wrist. 

*  A  long  pause  of  a  respiratory  arrhj'thmia  occurring  during  expiration 
may  be  mistaken  for  intermittence  if  the  examination  is  cursory. 

t  Sometimes  the  pauses  following  the  pairs  are  not  of  uniforin  length. 
The  irregularity  is  then  a  complex  one  ;  it  is  due  to  auricular  fibrillation,  to 
which  premature  beats  have  been  added.  Patients  who  show  it  are  usually 
under  the  influence  of  excessive  doses  of  digitalis. 


Disorders  of  the   Cardiac  Mechanism.  7 

Halved  pulse  rate.  When  the  ventricle  beats  at  twice 
the  pulse  rate,  the  disorder  is  due  to  premature  contractions 
in  all  but  the  rarest  instances.  Alternation  has  been  known 
to  occasion  halving,  the  weak  alternate  beats  failing  to  reach 
the  wrist  ;  but  this  condition  is  of  great  rarety  and,  when  it 
occurs,  is  very  transient.  The  two  are  readily  differentiated^ 
for  in  the  first  instance  the  ventricular  beats  are  coupled, 
while  in  the  last  they  appear  regularly. 

When  sudden  and  exact  halving  of  pulse  rate  is  noted  and 
the  ventricular  rate  is  halved  simultaneously,  the  disorder  is 
the  result  of  heart-block. 

A  grossly  irregular  j^ulse  in  which  there  is  an  intricate 
admixture  of  stronger  pulsations  with  C[uick  runs  of  almost 
imperceptible  beats,  and  in  which  the  lengths  of  intervening 
pauses  are  constantly  varying,  is  due  to  auricular  fibrillation. 

A  mild  grade  of  irregularity  which  persists,  which  is  not 
related  to  respiration  even  when  the  breathing  is  deepened 
and  in  which  no  definite  sequence  of  events  can  be  determined, 
is  also  due  to  auricular  fibrillation  in  most  cases.  A  similar 
irregularity  which  shows  relation  to  respiration  is  a  sinus 
arrhythmia. 

Familiarity  with  the  few  rules  which  I  have  no\v  given 
will  enable  the  practitioner  to  identify  most  forms  of  disorderly 
heart  action  with  which  he  meets.  But  when  he  is  in  doubt, 
or  when  he  requires  more  explicit  information,  in  regard  to 
the  arrangement  of  the  beats,  or  in  respect  of  the  management 
of  the  case  in  which  the  disorder  is  discovered,  he  may  refer 
to  the  more  precise  descriptions  contained  in  the  foUo^^ing 
chapters. 


(  «  ) 


Chapter   ir. 

SINUS   IRREGULARITIES. 

Definition. 

Irregularities  of  the  heart  which  are  jDroduced  by 
interferences  with  the  rhythmic  impulses  at  the  seat  of  their 
discharge. 

The  nature  of  sinus  disturbances. 

In  a  discussion  of  sinus  irregularities,  the  nerve  supply 
of  the  heart  in  relation  to  disturbances  of  rhythm  occupies  a 
prominent  place.  Let  me  state  emphatically  at  the  outset 
that  we  have  nothing  to  do,  first,  with  the  functions  of  the 
intrinsic  cardiac  ganglia,  nor,  secondly,  with  the  sympathetic 
nerve  trunks  ;  as  we  have  little  knowledge  of  the  part  they 
play  in  disease,  so  any  hypothesis  which  ascribes  a  derange- 
ment of  the  heart  to  perversion  of  their  functions  is  without 
practical  significance.  We  have  a  limited  but  real  knowledge 
of  the  vagus  and  its  relation  to  pathology  ;  my  remarks 
upon  the  cardiac  nerves  are  consequently  confined  to  it. 

The  complete  beat  of  the  normal  heart  consists  of 
a  contraction  of  its  chambers  in  orderly  sequence.  The 
wave  of  contraction  has  been  proved  to  start  in  a  small 
mass  of  tissue,  the  sino-auricular  node  (Fig.  1),  which  lies 
embedded  near  the  upper  and  anterior  end  of  the  sulcus  termin- 
alis.  The  sulcus  terminalis  runs,  as  may  be  remembered, 
from  the  junction  of  the  right  auricular  appendix  and  superior 


Sinus  arrhythmia. 


9 


vena  cava  towards  the  inferior  vena  cava  (see  Fig.  1).  The 
tissue  of  the  node,  consisting  of  a  network  of  small  spindle- 
shaped  muscle  cells,  richly  supplied  by  the  nerves  of  the  heart 
which  enter  in  this  region,  lies  therefore  at  the  mouth  of  the 
superior  vena  cava  and  is  embedded  in  the  wall  of  the  right 


Sup  Vena  Cava 


3IN0-AURICULAR 
Node 


Sulcus  TerminaliS. 

AuRicuLO  Vent  Bundle 
Left  Branch 

.         Foramen  Ovale 

>\uriculo-ve.mt. 
Node 

CoBONARv  Sinus 
Tr  icospio  Valve 


I  Nt  Vena  Cava 


Fig.  1.  A  diagram  of  a  human  lieart.  The  walls  of  inferior  vena  cava,  right 
auricle  and  right  ventricle,  have  been  partially  removed  to  expose  the 
septa.  The  position  of  the  sino -auricular  node,  in  which  the  heart  beat 
commences,  is  shown,  as  are  also  the  position  of  the  auriculo -ventricular 
node  and  the  course  of  the  auriculo -ventricular  bimdle  and  its  branches. 
The  last-named  structures  convey  the  contraction  wave  from  auricle 
to  ventricle. 

auricle.  The  contraction  which  commences  in  its  neighbour- 
hood spreads  through  the  walls  of  both  auricles  and  is 
transmitted  to  the  ventricles  by  a  special  band  of  tissue 
which  will  receive  subsequent  description.  The  orderly 
rhythm  of  the  whole  heart  takes  its  origin  in  this  node,  to 


10  Chapter    II. 

which  I  have  consequently  applied  the  term  heart's  "  pace- 
maker." In  the  normally  acting  adult  heart  the  pacemaker 
sends  forth  waves  of  contraction  at  rates  which  average  72 
per  minute,  and,  the  separate  beats  being  evenly  spaced,  the 
systoles  follow  each  other  in  a  regular  order  or  rhythm.  The 
pacemaker  is  under  the  control  of  the  vagi,  or  inhibitory 
nerves  of  the  heart,  and  these  normally  restrain  this  stimulus 
producing  centre,  holding  it,  as  it  were,  in  leash.  Destruction 
of  the  nerves,  more  especially  that  of  the  right  side,  or  the 
administration  of  atropine,  which  paralyses  the  nerve  endings- 
in  the  heart,  raises  the  rate  at  which  the  heart  beats  follow 
each  other.  In  the  human  subject,  the  probable  limit  to 
which  the  rate  may  rise  as  a  result  of  this  denervation  i& 
150-160  per  minute. 

In  many  subjects  under  special  conditions,  the  vagus 
curbs  the  heart  excessively,  and  this  over-action  of  the  nerve 
is  apt  to  be  relatively  constant  or  rhythmic.  There  conse- 
quently results  either  a  relatively  uniform  pulse  slowing  or  a. 
waxing  and  waning  of  heart  rate.  Let  us  deal  with  the 
persistent  slowing  first,  for  it  is  a  subject  Mdth  which  we  are 
only  briefly  concerned  in  these  chapters.  Pronounced 
slowing  of  the  whole  heart  is  comparatively  rare  ;  the  lesser 
grades  of  slowing,  many  of  which  are  of  vagal  origin,  slowing 
to  50  or  60  beats  per  minute,  are  not  uncommon  and  are 
especially  prominent  in  athletes  and  in  association 
with  increased  arterial  j)i'6S"'5ure,  pregnancy,  jaundice, 
convalescence  from  the  acute  fevers  and  less  frequently 
with  other  conditions.  Pulse  slowing  of  this  degree  has 
no  great  significance,  and  it  is  common  to  meet  with 
people  who  enjoy  perfect  health  and  in  whom  during 
rest  the  pulse  rate  habitually  lies  between  these  limits. 


Sinus  arrhythynia. 


11 


Periodic  or  varying  disturbances,  which  influence  the 
rhythm  of  the  heart  at  its  source  and  produce  a  greater  or  lesser 
degree  of  arrhythmia,  are  more  important,  though  only  the 
commoner  varieties  of  such  irregularity  need  to  be  described. 

In  Fig.  2  a  diagram  of  a  characteristic  sinus  arrhythmia 
is  given.  I  shall  refer  to  similarlj^  constructed  diagrams  in 
succeeding  chapters.  The  figure  is  arranged  so  that  each 
narrow  black  rectangle  {A)  represents  a  single  co-ordinate 
beat  of  the  auricle,  and  so  that  each  broad  black  rectangle  (  V) 
represents  a  co-ordinate  ventricular  contraction.     Where  an 


Fig.  2.  A  cliagTamn:iatic  representation  of  the  action  of  a  heart  affected 
by  sinus  arrhythmia.  The  contractions  of  auricle  and  ventricle  are 
represented  by  the  thin  and  broader  black  rectangles,  A  and  V  respec- 
tively. The  auricle  contracts  at  the  beginning  of  each  cycle,  and  sends 
its  impulse,  indicated  by  an  oblique  line,  to  the  ventricle,  which  responds. 
The  irregularity  consists  of  a  waxing  and  waning  of  rate,  in  which  auricle 
and  ventricle  participate  equally. 


auricular  contraction  is  followed  by  a  ventricular  response, 
an  oblique  line  is  drawn,  joining  the  corresponding  rectangles. 
The  slope  of  the  obhque  line  indicates  the  time  interval 
between  the  contraction  of  auricle  and  ventricle.  All  such 
diagrams  read  from  left  to  right.  In  the  present  example,  a 
sinus  irregularity,  the  whole  heart  is  affected,  so  that  each 
ventricular  contraction  is  preceded  by  an  auricular  systole  at 
the  usual  interval.  The  irregularity  consists  of  a^  gradual 
waxing  and  waning  of  auricular  rate  which  is  repeated 
periodically,  and  which  is  followed  exactly  by  the  ventricle. 


12 


Chapter    1 1. 


Respiratory  irregularities. 

It  is  well  known  that  young  adults  manifest  a  verj- 
appreciable  irregularity  of  the  heart  and  pulse  action 
when  they  breathe  deeply  (Fig.  3).  The  pulse  quickens  when 
the  chest  is  inflated,  and  slows  when  the  chest  is  emptied. 
But  in  young  adults  and  in  the  aged  also  there  is  usually  no 
respiratory   variation   of   pulse   rate,    which   the   finger   can 


Fig.  3.  A  sphygmographic  curve  from  a  normal  subject,  breathing  deeply. 
There  is  an  increase  of  pulse  rate  during  inspiration  and  a  decrease  during 
expiration. 


■t  i>  M  I  »  il»  »»  » 


i»<'nm»  « I II  ''HH 


■  I     •  I     II 


Fig.  6.  A  gross  sinus  arrhythmia  of  rare  type  ;  a  long  pulse  cj'cle  accompanies 
each  expiration.  In  this,  as  in  all  similar  figures,  the  top  line  represents 
time  in  fifths  of  seconds. 


discover,  while  the  breathing  is  natural.  On  the  contrary,  a 
perceptible  degree  of  natural  respiratory  irregularity  of  the 
pulse,  characterised  chiefly  b}'  one  or  more  longer  pauses 
during  the  expiratory  period  (Figs.  4  and  5),  is  not  uncommon 
in  young  children,  and  sometimes  it  is  sufficiently  prominent  to 
attract  immediate  attention.     Irregularity  of  a  verj^  similar 


Sinus  arrhythmia. 


13 


14  Chapter   II. 

kind  is  found  frequently  at  the  age  of  puberty,  and  it  is  also 
seen  on  rare  occasions  in  the  adult  (a  striking  though  rare 
example  of  the  last  is  shown  in  Fig.  6). 

All  these  irregularities  are  of  vagal  origin. 

Sinus  irregularities  lohich  bear  no  relation  to  respiration. 

While  the  vagal  irregularities  of  heart  rhythm  generally 
show  a  respiratory  relation,  disturbances  of  similar  origin 
occur  where  there  is  no  association  between  the  changes  and 
the  several  acts  of  breathing.  These  disorders  of  the  heart 
fall  into  three  main  categories.  They  are  : — (1)  Sudden  and 
prolonged  cessation  of  the  whole  heart  beat  usually  associated 
with  syncope  ;  it  is  a  very  rare  condition  and  requires 
but  a  passing  notice  in  this  general  survey.  (2)  Relatively 
abrupt  and  profound  slowing  of  the  whole  heart  (to  20  or 
40  beats  per  minute),  accompanied  by  an  independent 
lowering  of  blood-pressure.  This  disturbance  is  often 
responsible  for  attacks  of  faintness  or  actual  loss  of  con- 
sciousness. I  have  met  with  it  frequently  in  soldiers  invalided 
for  the  condition  known  as  "  irritable  heart."  It  is,  I  believe, 
the  commonest  cause  of  fainting  attacks  in  men  and  women. 
(3)  Phasic  variation  of  pulse  rate,  in  which  a  retardation  and 
subsequent  gradual  acceleration  of  the  whole  heart  occurs  ; 
the  change  is  spread  over  ten,  fifteen  or  more  seconds,  and 
may  be  repeated  regularly  or  may  occur  from  time  to  time  ; 
it  is  associated  ynth.  the  administration  of  heavy  doses  of 
drugs  of  the  digitahs  group,  but  may  be  seen  apart  from  them 
(Fig.  7)  ;  it  is  an  uncommon  type  of  irregularity.  (4)  An 
irregularity  of  the  whole  heart  of  mild  degree,  in  which  shorter 
and  longer  pauses  are  mingled  indiscriminateh\  It  is  not 
infrequent,  and  is  almost  alwaj^s  combined  with  a  general 


Sinus  arrhythmia.  15 

reduction  of  pulse  rate.  It  may  be  found  in  quite  young  and 
a-pparently  healthy  children  (Fig.  8)  and  is  also  encountered 
in  young  adults  in  whom  no  other  cardiac  sign  is  apparent. 
It  is  specially  frequent  in  patients  who  have  rheumatic 
heart  disease  and  who  are  under  the  influence  of  digitalis  ; 
it  is  accentuated  when  the  heart  slows  after  it  has  quickened 
in  response  to  exercise. 

These  sinus  irregularities,  like  those  which  are  related  to 
respiration,  are  all  due  to  alterations  of  vagal  tone. 

The  recognition  of  sinus  irregularities. 

Sinus  irregularities  are  usually  recognised  with  ease. 
It  may  be  said  that  the  great  majority  of  pulse  irregularities 
Avhich  occur  before  the  end  of  the  first  decade  are  of  this 
land,  and  most  of  them  are  respiratory.  When  there  is 
the  definite  relation  to  respiration,  no  further  evidence  is 
required  ;  in  most  instances  of  sinus  irregularity  this 
relation  is  present,  but  if  it  is  absent  it  becomes  established 
if  the  breathing  is  deepened  ;  a  gradual  waxing  and  waning 
of  rate  is  always  highly  suggestive,  if  not  conclusive.  The 
radial  beats  and  apex  pulsations  correspond ;  the  heart 
sounds  are  simply  modified  according  to  the  incidence  of  the 
ventricular  contractions.  The  radial  beats  are  full,  and  the 
•apices  of  the  several  pulsations  maintain  an  almost  constant 
height  in  arterial  curves  (Figs.  4,  5  and  8). 

Vagal  irregularities  are  all  abohshed  by  any  factor  which 
notably  increases  the  average  pulse  rate.  Thus  they  disappear 
with  exercise,  with  fever,  or  shortly  after  the  administration 
of  amyl  nitrite  or  atropine.  Atropine  also  cuts  short  or 
prevents  standstill  of  the  heart  and  the  profound  slowing 
described  on  the  previous  page. 


16  Chapter    II. 

The  prognostic  significance  of  sinus  irregularities. 
The  commoner  form  of  sinus  irregularity  (excluding 
those  which  may  be  responsible  for  syncope  and  the  true 
phasic  variation  of  pulse  rate)  are  of  little  prognostic  value. 
They  are  so  frequent  in  patients  who  present  no  other  sigit 
of  cardiac  disturbance,  either  at  the  original  examination " 
or  subsequently,  that  they  are  to  be  regarded  either  as 
slight  exaggerations  of  a  normal  phenomenon  (respiratory 
irregularity)  or  as  evidences  of  a  mild  and  insignificant 
instabiUty  of  tonic  inhibitory  nerve  action.*  Unhappily, 
different  forms  of  cardiac  irregularity  are  still  widely  confused; 
irregular  action  of  the  heart  in  children  is  still  regarded  by 
many  as  a  grave  sign  ;  it  is  usually  a  phenomenon  of  health 
and  when  of  sinus  origin  may  be  disregarded  safely.  The 
common  sinus  irregularities  should  not  be  allowed  to  influence 
the  habits  of  those  who  exhibit  them  ;  they  neither  suggest 
nor  require  special  therapy. 


*  Occurring  in  children,  this  irregularity  has  obtained  without  reason  an 
unenviable  reputation,  on  account  of  its  supposed  relation  to  tuberculous, 
meningitis. 


17 


CHAPTER    in. 

HEART-BLOCK. 

Definition. 

An  abnormal  heart  mechanism,  in  which  there  is  a 
delay  in,  or  absejice  of,  ventricular  resporises  to  the  auricular 
impulses^ 

The  nature  of  heart-block. 

Under  normal  circumstances,  the  ventricle  depends  for 
its  stimulus  upon  impulses  which  are  sent  down  to  it  from 
the  regularly  contracting  auricle.  Each  auricular  systole 
transmits  a  stimulus  to  the  ventricle,  and  this  stimulus 
travels  from  auricle  to  ventricle  along  a  narrow  neuro- 
muscular path,  the  auriculo-ventricular  bundle.  This  band 
of  tissue  starts  in  the  right  auricle  near  the  coronary  sinus 
and  proceeds  forwards  and  downwards  to  the  membranous 
septum  of  the  ventricle  (Fig.  1),  where  it  divides  into  two 
main  branches  on  either  side  of  the  septum.  The  main 
branches  subdivide  and  are  connected  to  the  ventricular 
musculature  through  the  complex  network  of  cells  named  after 
Purkinje.  The  sequence  in  which  the  chambers  of  the  heart 
normally  contract  is  diagrammatically  illustrated  by  Fig.  9. 

When  from  any  cause  the  function  of  the  tissues  uniting 
auricle  and  ventricle  is  impaired,  this  sequential  contraction 
is  disturbed.  The  grades  of  disturbance  which  human 
hearts  manifest  are  numerous. 


18  Chapter    III. 

There  may  be  a  simple  prolongation  of  the  interval 
which  separates  the  beginnings  of  auricular  and  ventricular 
systole  (the  As-  Vs  interval,  as  it  is  termed).  Such  a  con- 
duction defect  is  illustrated  by  Fig.  10  ;  the  thin  lines  become 
more  obhque  in  the  diagram,  and  a  gap  is  left  between  the 
end  of  auricular  and  the  beginning  of  ventricular  systole. 


Fig.   9.  Fio.   10. 

Fig.  9.  A  diagram  representing  the  normal  heart  action.  Tlie  auricle  con- 
tracts first  and  transmits  an  impulse  (represented  by  the  oblicjue  line)  to 
the  ventricle.  The  ventricle  responds  and  commences  to  contract  imme- 
diately at  the  cessation  of  auricular  systole. 

Fig.  10.  A  diagram  illustrating  the  earliest  stage  of  heart-block.  An 
interval  appears  between  the  end  of  auricxilar  and  the  commencement  of 
ventricular  systole.  There  is  delay  in  the  transmission  of  the  iinpulse 
from  auricle  to  ventricle  (indicated  by  the  increased  obliquity  of  the  line 
which  joins  the  rectangles  in  the  diagram). 


Where  the  grade  of  heart-block  is  higher,  the  ventricle 
may  fail  to  respond  to  occasional  auricular  impulses  ;  a 
condition  commonly  designated  b}^  the  term  "  dropped  beats." 
This  form  of  heart-block  is  rarely  a  simple  phenomenon  ;  it  is 
almost  always  complicated  by  variations  in  the  lengths  of 
As  -  Vs  intervals  over  the  period  of  disturbance.  The 
relation  of  chamber  contractions  may  be  studied  in  Fig.  11. 
A  "  dropped  beat  "  or  ventricular  silence  produces  a  pause 
of  exceptional  length  and  this  pause  breaks  the  natural 
rhythm  of  the  A^entricle.  Where  there  is  no  associated 
variation  in  the   As-  Vs  intervals,  the  long  ventricular  cycle 


Heart-block.  19 

is  necessarily  equal  to  that  of  two  regular  cycles.  But 
this  is  rarely  the  case  ;  the  "  dropped  beat  "  is  foreshadowed 
by  a  progressive  increase  of  the  preceding  As-  Vs  intervals 
(Fig.  11,  1,  2  and  3).  Moreover,  the  As-  Vs  interval  which 
follows  the  silence  is  generally  curtailed  (Fig.  11,  4).  These 
changes  in  the  conduction  intervals  shorten  the  long  ventri- 
cular cycle  and  consequently  diminish  the  grade  of  ventricular 
disturbance.  The  exact  manner  in  which  the  changes 
happen  requires  closer  study.  Consider  the  first  three 
As-  Vs  intervals  of  Fig.  11  ;  as  illustrated  by  the  obliquity 
of  the  Hnes,  the  interval  gradually  widens,  but  it  widens 
in  a  peculiar  manner.      The  increase  of  the  second  interval 


Fig.  1 1.  The  second  stage  of  heart-block,  to  which  the  term  "  dropped  beats  " 
is  appUed.  Up  to  the  point  where  the  chief  disturbance  occurs,  the  gaps 
between  the  auricular  and  corresponding  ventricular  contractions  widen 
out.  The  impulses  travel  to  the  ventricle  with  increasing  difficulty.  The 
fourth  auricular  contraction  stands  isolated,  it  yields  no  response  ;  a 
ventricular  contraction  is  "dropped."  Following  the  ventricular  pause, 
the  As-  Vs  interval  is  short,  for  the  tissues  have  rested,  but  it  agaiii 
widens  as  successive  cj^cles  follow. 


I   I    I  I 
\      I 


Fig.    12.     A  diagram  of  2  :  1  heart-block,  in  wluch  the  ventricle  responds  to 
each  second  auricular  beat. 


20  Chapter   III. 

over  the  first  is  greater  than  the  increase  of  the  third  over  the 
second.  The  result  is  a  decrease  of  the  interventricular 
period  directly  preceding  the  ventricular  silence.  The 
ventricle  quickens  to  the  point  of  the  disturbance.  The 
shortening  of  the  .4^-  Vd  interval  following  the  pause,  and  the 
subsequent  prolongation  of  it,  produces  a  similar  quickening 
of  the  ventricle  after  the  disturbance.  The  primary  and 
.secondary  accelerations  of  ventricular  rate,  before  and  after 
the  disturbance,  help  to  identify  the  disorder  in  many  arterial 
curves  of  heart-block. 

As  the  grade  of  heart -block  rises,  and  ventricular 
silences  become  more  frequent,  relatively  simple  ratios  are 
established  between  the  auricular  and  ventricular  rates. 
When  the  ventricle  beats  at  only  half  the  rate  of  the  auricle, 
because  alternate  impulses  are  ineffective,  the  condition  is 
spoken  of  as  2  :  1  heart-block  (Fig.  12).  3  :  1  and  4  :  1 
ratios,  in  which  each  third  or  fourth  auricular  impulse  alone 
yields  a  ventricular  response,  are  sometimes  encountered, 
but  they  are  uncommon. 

The  disturbances  which  have  been  described  are  all 
included  under  the  term  "  partial  heart-block." 

I  I  I  I  I  I  I  I  I 


III     I    I     I 

Fig.  13.  A  diagram  of  complete  heart-block  or  dissociation.  Both  the 
auricle  and  the  ventricle  beat  regularly,  but  at  independent  rates.  The 
relative  positions  of  auricular  and  ventricular  contractions  are  very 
variable. 


Heart-block.  21 

The  highest  grade  of  heart-block  is  reached  when  no 
impulses  are  transmitted  to  the  ventricle.  When  this 
happens,  the  ventricle,  having  completely  lost  the  controlling 
influence  of  the  auricle,  beats  in  response  to  a  slow  and 
regular  series  of  impulses  which  it  builds  up  intrinsically. 
In  "  complete  heart-block  "  or  "  dissociation  "  two  entirely 
separate  rhythms  are  maintained  ;  one  starts  in  and  controls 
the  auricle,  the  other  originates  in  and  regulates  the  ventricle. 
The  first  has  the  usual  rate,  72  per  minute  or  thereabout  ; 
the  last  has  an  approximate  rate  of  30  to  the  minute. 
Though  both  are  regular,  the  rhythms  are  mutually  indepen- 
dent (Fig.  13)  and  the  systoles  of  auricle  and  ventricle  fall 
with  varying  time  relations  to  each  other. 

Etiological  and  pathological  associations. 

Age  and  sex.  Heart-block  may  occur  at  any  age.  It 
has  been  observed  in  the  newborn  child  and  at  almost  all  ages 
into  the  eighties  and  nineties.  Its  age  distribution  is  settled 
by  the  age  incidence  of  the  diseases  which  produce  it.  Thus, 
it  is  especially  prevalent  amongst  those  whose  hearts  have 
been  severely  damaged  by  rheumatic  fever  or  chorea, 
so  that  a  special  class  of  case  is  grouped  between  the  years 
10  and  35.  Senile  affections  account  for  another  large 
group  of  patients  who  suffer  from  this  cardiac  disturbance  ; 
these  patients  are  elderly.  But  the  causation  is  so  varied 
that  no  age  is  exempt. 

Heart-block  is  much  commoner  in  man  than  in  woman. 

Heredity.  A  single  instance  of  the  supposed  occurrence 
of  several  cases  of  heart-block  in  the  same  family  has  been 
reported,  but  has  not  been  substantiated.  It  is  highly 
improbable    that    heredity    plays    any    direct    part    in    the 


22  Chapter   111. 

affection  ;  though  a  few  cases  of  congenital  heart-block  a'i-e 
on  record. 

Relations  to  infeciive  disease.  Relatively,  heart-block 
is  not  infrequent  during  the  course  of  infective  diseases,  and 
of  these  rheumatic  fever  holds  the  first  place  ;  the  disturbance 
is  usually  temporary.  The  exact  relation  of  rheumatic 
affections  to  acute  and  sub-acute  inflammatory  lesions  of  the 
heart  is  but  imperfectly  known,  but  there  is  a  clear  connection 
between  them.  Many  instances  of  heart-block  have  been 
reported  during  the  course  of  severe  rheumatic  fever  and  its 
compUcations,  acute  endocarditis  and  pericarditis.  It  is  pro- 
bable that  the  infection  of  the  heart  is  never  Umited  to  its  outer 
or  inner  layer  ;  the  middle  layer  or  myocardium  is  probably 
always  involved.  My  own  experience  leads  me  to  think 
that  heart-block  is  almost  a  common  accompaniment  of 
acute  or  sub-acute  rheumatism  of  the  heart,  for  I  have  seen 
a  number  of  patients  in  whom  during  the  course  of  rheumatic 
fever  involving  the  valves  or  pericardium,  or  both,  dropped 
beats  or  partial  heart-block  in  its  several  grades  have  been 
present.  In  other  instances,  temj^orary  heart-block  has 
appeared  during  short  febrile  attacks  in  patients  who  have 
been  previously  affected  by  rheumatic  fever.  It  is  certain 
that,  being  transient,  it  is  often  overlooked. 

Other  acute  affections  which  should  be  mentioned  are 
those  of  the  more  active  pus  organisms,  and  also  those  of 
diphtheria,  influenza,  typhoid,  scarlet  fever  and  pneumonia  ; 
heart-block  in  these  conditions  is  limited  to  infections  of 
severity. 

A  large  proportion  of  the  reported  cases  of  chronic 
heart-block  and  of  those  which  have  come  under  my  own 
observation,  have  belonged  to  two  groups  ;  the  disorder  has 


Heart-block.  23 

followed  single  or  repeated  attacks  of  rheumatic  fever,  or 
has  been  the  direct  result  of  syphihs.  Whether  of  rheumatic 
or  syphilitic  origin,  whether  acute  or  chronic,  heart-block  is 
generally  but  an  expression  of  a  widespread  affection  of  the 
heart  muscle  in  these  patients,  though  the  lesion  may  be 
confined  to,  or  may  fall  most  heavily  upon,  the  tissues  which 
establish  functional  connection  between  the  auricle  and 
ventricle.  In  a  fourth  of  the  cases  in  which  the  hearts  have 
been  secured  after  death  the  lesion  has  been  gummatous. 
In  a  series  of  42  cases  which  I  collected  in  a  few  years,  6  gave 
a  frank  history  of  venereal  infection  and  14  a  history  of 
rheumatism. 

The  relation  of  heart-block  to  rheumatism  in  chronic 
heart  affections  is  a  peculiar  one.  The  heart-block  is  often 
dormant  or  is  detected  only  by  exact  instrumental  methods  ; 
it  may  be  unmasked  by  the  administration  of  drugs  of  the 
digitalis  group,  for  the  higher  grades  of  heart-block  are 
produced  from  the  lesser  by  these  poisons. 

Relation  to  chronic  degenerative  processes  of  more  obscure 
origin.  Many  cases  of  heart-block  are  in  elderly  people, 
and  observation  shows  that  the  responsible  damage 
is  part  and  parcel  of  a  widespread  change,  either  in  the 
heart  alone,  or  in  the  heart  and  its  vessels.  A  number 
of  the  lesions  can  undoubtedly  be  traced  to  syphilis 
or  rheumatism,  but  the  cause  of  a  still  larger  number 
is  obscure.  Chronic  inflammation,  fibrosis^  atrophy,  cal- 
cification or  fatty  degeneration  of  the  tissues,  associated 
or  unassociated  with  disease  of  the  coronary  arteries,  are 
amongst  the  most  frequent  causes. 

Heart-block  as  the  result  of  digitalis  administration.  I 
have  referred  to  the  unmasking  of   dormant  heart-block  in 


24  Chapter   III. 

rheumatic  heart-disease.  When  digitahs,  or  an  alhed  drug 
such  as  strophanthus  and  squills,  is  given  in  toxic  doses  to 
young  patients  who  have  rheumatic  hearts,  it  is  not  uncommon 
to  observe  the  severer  grades  of  partial  heart -block  as  a  sequel. 
In  most,  but  not  all,  of  the  cases  which  react  in  this  manner 
a,  slight  defect  in  the  conduction  of  impulses  from  auricle 
to  ventricle  was  present  before  the  drug  was  taken.  The 
added  effect  may  be  due  to  the  action  of  digitalis  upon  the 
vagus  nerve,  for  sometimes  it  can  be  removed  by  atropine. 

Heart-block  may  be  induced  in  experiment  by  stimulating 
the  vagus,  and  efforts  have  been  made  to  estabhsh  a  chnical 
group  in  which  the  heart-block  is  attributable  to  disturbed 
innervation.  Up  to  the  present  time  there  is  no  very  clear 
evidence  that  anything  but  a  temporary  disturbance  of  this 
character  may  be  initiated  purely  by  vagal  impulses  ;  though, 
as  I  have  stated,  a  pre-existing  tendency  may  be  exaggerated 
in  this  manner  ;  if  the  higher  and  enduring  grades  of  heart- 
block  are  ever  due  to  derangement  of  the  vagi,  this  form  is 
so  rare  that  it  scarcely  needs  consideration  in  practice. 

Special  morbid  anatomy.  It  is  in  the  main  bundle,  or  in 
its  auricular  attachment,  that  the  lesions  responsible  for 
heart-block  are  found.  The  kind  of  lesion  has  been  spoken 
of  already  Cummata,  chronic  inflammatory  processes  and 
their  accompaniments,  fibrosis,  atrophy,  and  calcification 
arejnpst .frequently  seen.  Examples  of  tumours  (fibroma 
and  endothelioma)  affecting  these  special  tissues  have  been 
recorded. 

Ulceration  invading  the  bundle  (rarely),  acute  inflamma- 
tion evidenced  by  deposition  of  leucocytes  (commonly),  or 
parenchymatous  degeneration  of  the  bundle  are  the  lesions 
found  in  hearts  damaged  by  acute  or  subacute  infections. 


Heart-block.  25 

The  recognition  of  heart-block. 

The  disorders  of  the  heart's  mechanism  caused  by 
heart-block,  in  its  several  grades,  are  readily  recognised  by  the 
exact  graphic  methods  provided  by  the  ^polygraph  and 
galvanometer.  The  efficacy  of  these  instruments  and  the 
certain  analysis  which  they  provide  must  be  evident,  for 
heart-block  produces  deranged  sequence  in  the  contractions  of 
auricle  and  ventricle,  and  the  polygraph  and  galvanometer 
supply  separate  and  clear  records  of  the  systoles  of  upper 
and  lower  chamber.  To  compare  the  onsets  of  the  several 
T  systoles,  therefore,  is  relatively  simple  when  these  recording 
■devices  are  employed. 

But  I  speak  to  those  to  whom  special  methods  are  not 
available,  and  I  hope  to  show  that  heart-block  can  be 
recognised  in  many  of  its  grades  by  simpler  means.  It  will 
be  necessary  to  treat  each  grade  of  the  disorder  separately. 

Often  the  earliest  manifestations  of  heart-block  consist 
in  a  widening  of  the  As-Vs  interval  (see  page  18) ;  this  defect 
•can  rarely  be  identified  by  ordinary  clinical  means  ;  yet 
it  may  be  responsible  for  two  physical  signs.  It  may  not  be 
known  to  everyone  that  auricular  systole  produces  a  distinct 
though  muffled  sound,  and  that  while  this  sound  is  inaudible 
when  the  heart's  mechanism  is  normal,  it  is  frequently  heard 
when  the  auricular  and  ventricular  systoles  are  sufficiently 
separated.  A  slight  widening  o£  the  As-  Vs  interval  may 
lead  to  a  redupUcation  of  the  first  heart  sound  ;  a  more 
pronounced  widening  may  result  in  a  double  second  sound, 
ior  the  auricular  systole  will  then  faU  in  early  diastole. 

Another  sign  is  confined  to  cases  of  mitral  stenosis  and 
is  of  similar  origin  ;  in  these  patients  the  systole  of  the  auricle 


26  Chajilcr   III. 

causes  or  reinforces  the  diastolic  rumble  Avhich  characterises- 
the  valve  lesion.  Contraction  of  the  auricle  at  an  abnormal 
instant  in  diastole  (for  example,  mid-diastole)  is  accompanied 
by  a^aurmur  and  thrill  at  a  corresponding  time.  When  the 
pulse  is  regular,  apical  thrills^r  rough  murmurs,  confined  to- 
mid-  or  early  diastole,  are  physical  signs  which  should  suggest^ 
not  alone  stenosis,  but  also  the  beginning  of  heart-block. 

Single  dropped  beats  are  not  difficult  to  detect.  Tak& 
the  case  of  a  pulse,  which  though  it  seems  otherwise  regular,  is- 
interrupted  by  an  occasional  pause  of  unusual  length,  while 
examination  of  the  cardiac  impulse  reveals  neither  movement 
nor  sound  in  the  pause.  If  the  pause  is  not  associated  regularly 
mth  the  expiratory  phase  of  respiration  (see  page  12)  it  can  be 
attributed  to  a  failure  of  the  customary  response  of  ventricle  to- 
auricle.  The  length  of  the  pause  in  radial  tracings  may  be 
exactly  equivalent  to  that  of  two  rhythmic  beats.  More- 
frequently  (as  in  the  radial  pulse  tracing  of  Fig,   14)  it  is- 


Fig.  14.  A  pulse  curve  showing  "  dropped  beats."  The  arrows,  which 
represent  the  positions  of  the  regular  aviricular  contractions,  have  been 
accurately  determined  in  this  and  subsequent  figures  by  means  of  poly- 
graphic  curves.  There  is,  of  course,  a  big  delay  between  the  auricular 
systole  and  the  pvilse  beat.  The  heart  sounds  are  shown  diagrammatically. 
The  arrangementof  the  jnilse  beats  depends  upon  the  lengths  of  the  As-  Vs- 
intei'vals  and  upon  the  failure  of  response  at  the  points  marked  by 
asterisks.  Note  the  widening  of  the  .45-  Vs  intervals  and  accompanying 
increase  of  pulse  rate  before  and  after  each  dropped  beat. 


distinctly  short  of  this,  and  is  preceded  and  succeeded  by 
slight  pulse  quickening.  The  nature  of  these  changes  has  been, 
considered    (page    19),   and   the   mechanism   is  indicated   in 


Heart-block. 


27 


the  present  figure  by  arrows  showing  the  points  at  which 
the  regular  auricular  systoles  fell.  Responses  to  the  auricular 
contractions  marked  by  asterisks  have  failed. 

With  exercise*  the  pulse  accelerates  and  becomes  regular  ; 
with  rest  the  irregularity  reappears  and  the  first  sign  of  its 
return  is  the  occurrence  of  an  unusually  long  ventricular  pause. 

When  dropped  beats  are  more  frequent,  the  irregularity 
takes  the  form  seen  in  Fig.  15.     Here  each  third  or  fourth 


Fig.   15.     Curves  of  heart's  apex  beat  and  pulse  from  a  patient  in.  whom 
ventricular  responses  failed  frequently. 

impulse  miscarries,  and  the  heart  and  pulse  beats  are  grouped 
in  twos  and  threes.  This  irregularity,  like  the  last,  may  be 
recognised  clinically  by  observing  the  action  of  the  ventricle 
immediately  at  the  end  of  exercise,*  for  it  is  abolished  when 
the  heart  rate  is  raised  and  its  resumption  is  signalled  by  a 
ventricular  pause,  as  opposed  to  a  premature  beat,  such  as  is 
heard  in  the  corresponding  extrasystolic  irregularity  in 
similar  circumstances  ;  the  same  test  apphes  to  such  irregu- 
larities as  are  seen  in  Figs.  16  and  17. 

2  : 1  heart-block  is  to  be  suspected  in  any  patient  in 
whom  the  ventricle  beats  regularly  and  in  whom  the  heart 
rate  hes  between  40  and  50  contractions  to  the  minute.  A 
sudden  and  exact  halving  of  ventricular  rate  is  always  most 
suggestive  of  its  onset.  2  :  1  heart-block  is  unstable,  the 
ventricle  quickening  from  time  to  time,  and  these    changes 

*0r  a  whiii  6f  amyl  nitrite. 


28 


Chapter    III. 


in  the  rate  of  its  response  to  auricle  disclose  the  nature  of 
the  whole  disturbance. 

Exercise*  abruptly  doubles  the  ventricular  rate  ;  with 
subsequent  rest  the  raised  rate  falls  abruptly  to  one  half. 

In  mitral  stenosis  partial  heart-block  is  often  character- 
ised  by    pecuharities    of   the    murmurs.        They    are    often 


Fig.  16.  Curves  of  heart's  apex  beat  and  pulse,  taken  during  the  transition 
from  frequent  "  dropped  beats  "  to  2  :  1  heart-block.  The  rate  is  reduced 
to  exactly  three-fourths  the  original  at  the  change. 


17.  Curves  showing  the  interruption  of  a  period  of  2  :  1  heart-block 
by  a  single  response  of  the  ventricle  to  one  of  the  series  of  alternate 
impulses  which  usually  yield  no  ventricular  contraction. 


The  transition  between  2  :  1  heart-block  and  an  arrangement  previously 
studied,  namelj%  the  loss  of  each  third  response,  is  shown  in  Fig.  16.  A 
bigeminal  or  covipled  action  of  the  ventricle  passes  over  into  a  slow  regular 
action.  The  features  which  proclaim  heart -block  in  this  curve  are  the  increase 
in  the  length  of  cycle  b  as  compared  to  a,  and  the  exact  reduction  of  rate  to 
three -fourths.  The  lengths  of  the  several  pauses  are  understood  by  examining 
the  positions  of  the  auricular  systoles  which  have  been  indicated  by  arrows 
drawn  on  the  curve.  Systoles  2a,  4a,  5a,  6a  and  7a  do  not  affect  the  ventricle  ; 
and  where  the  ventricle  is  silent  a  lengthy  pause  is  found.  The  arterial 
cycle  a  is  brief  as  compared  with  b  because  the  auricular  impulse  4  takes 
longer  to  reach  the  ventricle  than  does  impulse  5.  Disturbance  of  a  2  :  1 
period  is  shown  in  Fig.  17.  An  early  contraction  of  the  ventricle  is  followed 
by  a  pulse  cycle  a  which  is  shorter  than  b  and  the  succeeding  cycles.  The 
reason  of  this  shortening  has  been  explained  in  the  descriiDtion  of  the  last 
figure.  In  Fig.  17  heart-block  is  also  evidenced  by  the  total  duration  (c) 
of  the  two  short-cycles  ;  it  is  equal  to  one  and  a  half  times  that  of  the  longer 
cycles  (period  d).  In  other  words,  c  and  d  each  corres^^ond  to  three  auricular 
cycles. 

*  Or  a  whiff  of  amyl  nitrite. 


Heart-block. 


29 


extremely  complex.  Where  2  :  1  heart-block  is  present  two 
thrills  and  two  diastolic  murmurs  may  accompany  each 
ventricular  cycle.  The  arrangement  of  the  murmurs  will  be 
understood  when  it  is  remembered  that  the  thrill  and  harsh 
murmur  of  mitral  stenosis  are  produced  largely  by  auricular 


Fig.  18.  Ai'terial  and  apex  curves  from  a  case  of  mitral  stenosis,  while  there 
is  a  transition  from  dropped  beats  to  2  :  1  heart-block.  Note  the  arrange- 
ment of  the  diastolic  murmurs  and  their  dependence  upon  those  auricular 
contractions  which  force  blood  into  the  ventricle. 


J  f 


ii^o^dioX 


Fig.  19.  Apex  and  radial  curves  in  a  case  of  complete  heart-block.  The 
heart  sounds  are  modified  by  the  auricular  contractions,  which  are 
faintly  audible.  Where  auricular  and  ventricular  contractions  begin 
together  the  first  soimd  is  exaggerated.  The  pure  auricular  sounds  are 
shown  as  dots. 


systole^  and  that  in  2  :  1  block  the  auricle  contracts  twice  as 
frequently  as  the  ventricle.  A  more  complex  arrangement  of 
murmurs  is  illustrated  by  Fig.  18.  The  ventricle  beats  at  first 
in  couples,  and  at  such  times  the  murmur  occurs  before  the 
first  and  after  the  second  sound  of  the  first  beat  of  a  couple  ; 
the  second  beat  of  the  couple  is  accompanied  by  no  murmur, 
for  the  single  auricular  contraction  falling  in  its  neighbourhood 


30  Chapter   III. 

coincides  with  that  of  the  ventricle  and  forces  no  blood  through 
the  stenosed  orifice.  Over  the  last  portion  of  the  curve  2  :  1 
heart-block  is  present,  and  each  cycle  is  accompanied  by 
presystolic  and  early  diastolic  murmurs. 

In  complete  heart-block  the  action  of  the  ventricle  is 
phenomenally  slow  ;  nearly  all  hearts  which  beat  at  rates  of 
35  and  under  are  affected  in  this  manner.  The  rhythm  is 
generally  quite  regular.  The  rate  is  almost  or  quite  unaffected 
by  exercise,  or  by  the  administration  of  atropine  or  amyl 
nitrite.  Each  ventricular  beat  is  accompanied  by  a  first  and 
second  sound  ;  in  addition,  very  faint  muffled  sounds  are 
usually  to  be  heard  in  the  long  diastoles.  The  latter  are  due  to 
auricular  systoles.  A  sign  which  is  conclusive,  and  almost 
always  present,  is  a  changed  character  of  the  first  and  second 
heart  sounds  from  beat  to  beat.  When  the  auricular  and 
ventricular  contractions  begin  together,  the  first  sound  is  in- 
tensified, and  when  they  fall  almost  together  the  first  or  second 
sound  may  be  reduplicated  (Fig.  19).  Definite  and  recurring 
change  in  the  intensity  of  the  heart  sounds,  which  proves 
independent  of  respiration,  forms,  in  cases  of  slow  and 
regular  heart  action,  a  conclusive  sign  of  complete  heart- 
block.  Evidences  of  the  relatively  rapid  auricular  contrac- 
tion are  generally  seen  in  the  neck  ;  small  and  regular 
pulsations  (Fig.  20,  a  waves)  appear  in  the  jugular  veins 
between  the  beats  of  the  carotid  (c  waves).  From  time  to 
time  a  prominent  venous  pulsation  (Fig.  20,  ajc)  accompanies 
the  intensified  first  heart  sound,  when  auricular  systole 
coincides  with  that  of  the  ventricle  and  when  as  a  consequence 
the  blood  cannot  be  ejected  naturally  from  the  auricle.  A^ 
periodic  waxing  and  waning  of  the  venous  pulsations, 
independent    of    respiration,   is    always    highly    suggestive 


Heart-block. 


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32  Chapter   III. 

of  complete  block.  Traces  of  auricular  pulsations  upon 
the  arterial  curves  are  also  evident  in  most  of  the  patients 
from  whom  full  pulse  excursions  can  be  obtained  (Fig.  21). 
Where,  as  in  the  accompanying  figure,  the  little  waves  on 
the  downstrokes  of  the  regular  pulse  beats  show  a  gradual 
and  orderly  change  of  position,  moving  steadily  away  from 
the  succeeding  radial  upstroke,  the  presence  of  complete 
heart-block  is  certain. 

Effects  on  the  circulation  and  the  general  symptomatology. 

The  symptoms  suffered  by  the  subjects  of  heart-block 
are  divisible  into  two  groups.  On  the  one  side  are  those 
which  are  especially  associated  with  the  condition  itself, 
and  on  the  other  are  those  which  result  from  co-existing 
disease  in  other  parts  of  the  heart.  For  disease  is  rarely 
hmited  to  the  bundle,  and  generally  heart-block  is  but  a 
local  manifestation  of  a  more  widespread  process.  The 
effects  of  a  lesion  which  transects  the  bundle  differ  from 
those  of  a  similar  lesion  in  another  portion  of  the  musculature 
in  one  chief  respect  ;  the  lesion  so  placed  produces  manifest 
disturbance  ;  there  is  no  second  strand  which  may  fulfil 
the  functions  of  that  which  is  destroyed,  whereas  a  defect  in 
the  general  mass  of  muscle  is  hidden  by  the  response  of  the 
remaining  tissue.  As  in  disease  of  the  nervous  system,. 
where  large  masses  of  the  tissue  may  be  destroyed  without 
gross  outward  signs  of  damage,  but  where  a  minute  morbid 
focus  in  a  given  situation  gives  rise  to  obvious  and  profound 
disturbance,  so  it  is  with  the  heart.  It  should  be  emphasised 
that  heart-block  is  usually  an  indication  of  a  far  graver 
condition  than  simple  transection  of  the  bundle  ;  it  is  a 
sign  of  diffuse  invasion  of  the  myocardium. 


Heart-block.  33 

The  symptoms  produced  by  affections  of  the  whole 
heart  musculature  do  not  lie  within  the  scope  of  this  book  ; 
but  it  is  important  to  state  that  the  presence  of  heart-block 
demands  an  exhaustive  study  of  the  subject  in  whom  it 
appears  ;  in  all  instances  special  attention  should  be  directed 
to  the  fitness  or  otherwise  of  the  heart  as  a  whole. 
And  this  caution  is  not  limited  to  heart-block  ;  it  applies  to 
all  departures  from  the  normal  mechanism. 

The  special  symptomatology  of  heart-block  may  be 
conveniently  approached  from  two  standpoints. 

Heart-block  of  high  grade  is  accompanied  by  a  reduction 
of  the  rate  of  the  ventricle,  often  to  a  half  its  former  rate. 
What  is  the  effect  of  this  retardation  upon  the  circulation, 
and  what  are  the  results  of  the  lessened  nervous  control 
of  rate  which  accompanies  it  ?  It  is  certain  that  thereby  a. 
serious  burden  is  imposed  upon  the  efficiency  of  the  heart, 
as  a  pump  ;  but  nothing  is  more  remarkable  than  the 
accommodation  of  the  cardiovascular  system  to  conditions 
which  diverge  widely  from  the  normal.  Dissociation  of 
auricles  and  ventricles,  and  the  consequent  estabUshment 
of  a  slow  ventricular  rhythm,  is  followed  by  some  degree  of 
ventricular  hypertrophy.  No  doubt  this  increase  in  the  mass, 
of  the  ventricular  muscle  makes  up  in  a  measure  for  the  loss- 
of  co-ordination  and  of  the  natural  rates.  During  the  long 
diastoles  the  blood  is  squeezed  from  arteries  to  veins  and  a, 
low  diastolic  blood  pressure  results  ;  but  the  blood  pours 
equally  fast  from  veins  to  heart,  whose  chambers,  receiving 
the  extra  load,  expel  it  into  the  arteries.  Fullness  of  pulse 
and  high  systoUc  pressure  (170-200  mm.  Hg)  consequently 
characterise  the  arterial  system  when  in  persistent  heart- 
block  there  is  no  lack  of  healthy  cardiac  tissue.     In  evidence 


34  Chapter    III. 

of  the  adaptability  which  the  circulation  as  a  whole  shows 
to  the  new  conditions,  I  may  cite  the  case  of  a  patient  in 
whom,  judging  from  the  signs  and  symptoms,  the  damage 
to  the  muscle  mass  was  but  little.  The  patient,  a  man  of 
33  years,  was  known  to  have  had  a  heart  rate  of  30  to  35,  with 
occasional  accelerations  to  48,  for  15  years.  He  was  the  subject 
of  complete  heart-block.  There  was  a  little  hypertrophy  of  the 
heart,  but  no  subjective  symptoms.  He  led,  when  last  seen,  a 
very  active  business  Ufe,  and  passed  in  the  street  would 
have  been  judged  a  perfectly  healthy  person.  There  was  no 
circulatory  embarrassment,  even  after  strenuous  exertion  ;  he 
prided  himself  upon  his  sprinting  power  and  had  recently  run 
in  races.  An  instance  of  this  kind  offers  a  partial  answer 
to  the  original  questions  ;  the  slow  pulse  of  heart-block 
and  the  lost  regulation  of  rate  do  not  disable  an  otherwise 
healthy  heart  from  performing  its  full  work.  In  hearts 
more  profoundly  affected,  the  extra  burden  is  less  readily 
borne,  but  in  these  it  is  not  eas}^  to  dissociate  the  effects 
of  the  new  mechanism  from  those  of  disease  of  the 
remaining  muscle. 

In  the  second  place,  heart-block  is  responsible  for  a 
group  of  symptoms  arising  as  a  direct  result  of  excessive 
slowing.  Reduction  of  pulse  rate  beyond  certain  limits,  or 
the  check  to  the  arterial  flow  for  a  certain  time,  is  accom- 
panied by  grave  disorders  of  nutrition,  and  the  brain  is  an 
early  and  anxious  plaintiff.  The  patient,  who  exhibits 
conspicuous  pulse  slowing  in  conjunction  with  fits,  falls  into 
the  category  of  Adams-Stokes'  syndrome.  The  higher  grades 
of  heart-block,  whether  of  persistent  heart-block  in  which 
ventricular  responses  are  frequently  missed  (2:1,  3:1 
ratios,  etc.),    or    of    complete    dissociation,    are    frequently 


Heart-block.  35 

accompanied  by  temporary  periods  of  excessive  pulse  slowing 
or  by  cessation  of  the  ventricular  systole  for  prolonged 
intervals.  The  cause  of  change  in  the  ventricular  rate — 
the  auricles  continue  to  beat  at  the  usual  or  at  an  enhanced 
rate — is  not  fully  understood,  and  I  do  not  propose  to 
discuss  it.  The  symptoms  presented  by  the  patient  are 
intimately  dependent  upon  the  degree  of  heart  slowing  or 
upon  the  duration  of  isolated  periods  of  asystole.  When 
the  pulse  falls  to  8  or  20  beats  per  minute,  unconsciousness 
supervenes  ;  suspension  of  the  mental  functions  is  also 
produced  by  a  single  period  of  asystole  of  from  3  to  7  seconds' 
duration.  Patients  who  suffer  from  the  higher  grades  of 
heart-block  commonly  relate  a  history  of  brief  attacks  of 
giddiness,  fainting,  temporary  loss  of  consciousness  and  its 
dependent  accidents.  Seen  in  mild  attacks,  the  subject 
of  them  is  pulseless  and  momentarily  pale.  In  severer 
seizures,  where  the  pulse  ceases  for  15  seconds  or  more,  there 
are  additional  phenomena.  The  blood  is  dammed  back  in 
the  venous  system,  increasing  pallor  has  cyanosis  added  to 
it,  the  breathing  deepens  and  becomes  stertorous  ;  twitching 
of  the  face  and  upper  limbs  eventuates.  The  convulsive 
fit  rarely  spreads  beyond  the  described  area,  but  it  may 
become  more  generaUsed.  Urine  is  not  passed,  neither  is 
the  tongue  bitten  during  the  attacks.  In  most  cases  the 
condition  is  readily  recognised  by  the  silence  of  the  ventricle 
and  by  the  rapid  undulations  in  the  veins  of  the  neck,  signify- 
ing activity  of  the  right  auricle.  Unexpected  death  is  a 
by  no  means  uncommon  accident  amongst  the  affected,  but, 
considering  individual  attacks,  it  is  rare.  Death  occurs  after  a 
period  of  status  epilepticus  in  a  number  of  the  patients,  and 
the  status  consists  of  repeated  seizures  of  the  forms  described. 


36  Chapter   III. 

As  a  rule  the  patient  has  no  warning  of  an  impending 

syncopal  or  epileptic  attack  ;     though  on  occasion  he  or  his 

medical    attendant    may    be    informed    of    the    approaching 

danger  by  a  change  in  the  heart's  action,  for  example,  by  the 

occurrence  of  unusual  ventricular  slowing.     Such  sensations 

as  the  patient  may  experience  at  the  commencement  of  long 

seizures  are  similar  to  those  accompanying  a  brief  cessation 

of  the  heart  beat,  and  consequently  do  not  properly  constitute 

an  aura. 

The  prognosis. 

Heart-block  in  itself  does  not  kill  ;  those  who  suffer  or 
have  suffered  from  it  mostly  die  with  the  usual  symptoms  of 
general  heart  failure.  Let  me  be  clearly  understood  in  this 
statement.  Heart-block  and  the  Adams-Stokes'  syndrome 
are  by  no  means  synonymous  terms  ;  the  majority  of  patients 
who  exhibit  heart-block  never  have  fits,  for  the  higher  grades 
of  heart-block  are  not  common.  Lesser  grades  of  heart-block 
are  common  in  conjunction  with  rheumatic  heart  disease  ; 
they  produce  no  specific  symptoms.  Moreover,  the  syncope 
is  not  of  necessity  the  cause  of  death  even  in  chronic  heart- 
block  of  high  grade. 

The  prognosis  in  heart-block  has  to  be  dealt  mth  from 
several  points  of  view.  In  the  first  instance,  let  us  consider 
the  common  variety,  the  milder  grades  of  heart-block  such  as 
are  associated  with  rheumatic  heart  disease  (prolonged  As-  Vs 
intervals  or  "  dropped  beats  ").  Where  such  heart-block  is 
persistent,  there  are  usually  a  number  of  physical  signs  in 
addition  to  those  dependent  upon  disturbed  rhythm  or 
sequence  ;  they  are  the  signs  of  heart  disease,  muscular  or 
valvular,  in  its  several  and  universally  recognised  forms. 
Heart-block   is   often   the   least   prominent   phenomenon   in 


Heart-block.  37 

these  patients,  who  often  suffer  from  mitral  stenosis.  The 
only  question  that  I  raise  is  as  to  the  manner  in  which 
heart-block  affects  the  prognosis  in  these  cases.  It  should 
be  regarded  as  an  evidence  of  myocardial  damage,  not 
necessarily  limited  to  the  bundle,  but  probably  diffused 
throughout  the  heart.  My  experience  of  such  cases  is  that 
they  are  serious ;  in  fact,  most  of  those  I  have  seen  are  dead, 
though  they  have  not  died  of  heart-block.  But  temporary 
heart-block  of  mild  grade  is  not  uncommon  during  the  febrile 
attacks  to  which  rheumatic  heart  subjects  are  liable  ;  it 
occurs  also  in  pneumonia  and  typhoid  fever,  etc.  The 
appearance  of  this  abnormal  mechanism  is  of  importance, 
for  it  may  be  the  only  outstanding  sign  of  myocardial  damage. 
Whenever  it  complicates  an  acute  infection  it  consequently 
dulls  the  prognosis  ;  at  the  same  time  it  should  be  under- 
stood that  the  normal  mechanism  is  usually  recovered. 
Occurring  as  an  accompaniment  of  fever  in  a  patient  who 
has  rheumatic  heart  disease,  it  should  be  regarded  as  an 
outward  sign  of  an  isolated  injury  which,  if  often  repeated, 
eventually  so  weakens  the  muscle  that  life  is  no  longer 
supported. 

Where  the  higher  grades  of  heart-block  are  present,  the 
prognosis  is  based  upon  two  chief  considerations.  The 
general  evidence  of  the  integrity  and  fitness  of  the  muscle  as  a 
whole  should  be  weighed  first.  The  fits,  especially  their 
frequency  and  severity,  are  next  taken  into  account  ;  a 
number  of  the  patients  are  free  from  them  ;  others  are  in 
constant  peril ;  and  it  is  not  easy,  nay  it  is  often  impossible, 
to  predict  the  ultimate  effects  of  syncopal  attacks  or  severer 
crises  in  a  given  case.  Those  patients  especially  who  have 
progressive  lesions,  and  those  in  whom  partial  is  eventually 


38  Chapter    III. 

converted  to  complete  and  permanent  dissociation,  must 
pass  through  a  time  of  particular  danger  ;  for,  during  the 
passage  from  one  grade  of  block  to  the  other,  fits  are  very 
common  and  the  period  of  passage  may  not  be  a  short  one. 
It  is  useful  to  remember  also  that  those  who  have  partial 
heart-block  are  more  prone  to  fits  than  those  in  whom  the 
obstruction  is  complete.  Uncertain  in  both  incidence  and 
effect,  the  fits  always  dictate  a  cautious  prognosis. 

Regarded  in  its  entirety,  persistent  heart-block  of  high 
grade  is  a  grave  condition.  It  is  usviallj^  complicated,  and 
then  a  few  years  generally  close  the  scene.  Nevertheless, 
some,  and  especially  the  younger  patients,  survive  for  many 
years,  in  comparative  and  absolute  comfort.  These  are 
patients  in  whom  the  mass  of  heart  muscle  is  comparatively 
nealthy  and  in  whom  fits  are  rare  or  absent. 

The  treatment. 

In  all  cases  of  heart-block  a  careful  inquiry  into  the 
causation  is  to  be  undertaken,  it  if  is  not  obvious.  Syphilis 
as  a  possible  cause  in  middle  life  is  to  be  kept  in  mind 
especially. 

Persistent  heart-block  of  the  milder  forms  requires  no 
immediate  treatment,  but  is  an  indication  for  repeated 
examination  of  the  patients  who  show  it.  As  such  patients 
usually  require  treatment  for  the  general  condition  of  the 
heart,  constant  supervision  is  not  difficult.  Digitalis  medica- 
tion will  frequently  increase  the  grade  of  block.  The  increase 
of  block  should  not  deter  digitalis  administration,  for  it  is 
not  in  itself  detrimental  ;  the  drug  or  its  alKes  maj^  be 
given  without  restraint,  and  some  seem  to  receive  benefit 
from  it. 


Heart-block.  39 

When  the  abrupt  onset  of  partial  heart-block  is  observed,  it 
is,  as  I  have  said,  an  index  of  active  mischief.  The  patient 
should  remain  in  bed  and  should  be  thoroughly  searched  for 
the  provocative  cause,  which  is  attended  to  when  found. 
The  acute  infections  are  suitably  treated.  Rheumatic 
patients  are  treated  with  salicylates,  and  scrupulous  attention 
is  paid  to  the  hygiene  of  the  mouth  and  throat.  If,  after 
the  subsidence  of  remaining  symptoms,  the  block  remains 
and  persists  for  several  weeks,  the  patient  is  treated  along 
the  lines  indicated  in  the  previous  paragraph.  Heart-block 
in  itself  does  not  call  for  rest  in  bed  or  other  interference, 
though  a  suspicion  of  an  active  or  progressive  lesion  does. 

Full  exposure  to  open  air  has  been  advocated  and 
deserves  a  thorough  trial. 

The  higher  grades  of  heart-block  are  usually  chronic  and 
stationary  and  the  habits  of  the  patient  should  be  governed 
by  his  general  fitness.  Most  patients  of  this  class  are  up 
and  about,  and  are  able  to  undertake  many  of  their  ordinary 
duties  ;  yet  it  is  only  exceptionally  that  real  bodily  activity 
is  either  possible  or  permissible.  Here  again  a  suspicion 
that  the  lesion  is  active  or  progressive  calls  for  rest  and  careful 
watching.  A  history  or  sign  of  syphilis  constitutes  an 
imperative  demand  for  thorough  and  appropriate  treatment, 
and  in  some  cases  success  has  attended  the  administration  of 
mercurials  and  iodides  or  intravenous  treatment. 

All  those  who  have  fits  should  be  warned  of  the  danger 
which  they  run  from  accidents  during  these  attacks  if  they  do 
not  appreciate  it  fully.  Not  a  few  have  lost  their  lives  by  faUing 
heavily  or  in  traffic  and  suffering  mortal  injury.  In  many 
cases  the  fits  occur  in  groups,  and  additional  precautions  are 
required  until  such  attacks  cease.     Most  patients  have  brief 


40  Chapter  III. 

warnings  of  the  onset  of  unconsciousness,  and,  if  advantage  is 
taken  of  these,  less  risk  is  incurred. 

A  careful  inquirj'^  for  causes  predisposing  to  the  fits  may 
elicit  a  histor}^  of  gastro-intestinal  disturbance  or  over- 
^exertion,  upon  which  it  is  well  to  act. 

for  the  fit  ^^•hen  it  is  present  I  know  of  no  remedy 
which  is  of  avail  to  increase  the  pulse  rate  and  restore  the 
unconscious  patient.  Man}''  drugs  have  been  administered 
with  this  end  in  view,  and  the  list  includes  oxygen,  strychnine, 
strophanthine,  digitaUs  and  amyl  nitrite.  They  appear  to 
have  no  appreciable  effect.  Atropine  is  said  to  have  abolished 
fits  in  isolated  instances.  As  a  rule  it  is  contra-indicated. 
AdrenaHn  has  been  suggested  ;  I  know  not  if  it  is  of  value. 


(     41     ) 


Chapter  IV. 

PREMATURE  CONTRACTIONS  OR  EXTR ASYSTOLES. 

Definition. 

Contractions  of  the  heart  which  disturb  the  rhythmic 
sequence  by  appearing  early  and  in  response  to  impulses 
newly  formed  in  the  musculature. 

The  nature  of  premature  contractio7is. 

A  clear  conception  of  disordered  heart  action  can  be 
attained  only  by  those  who  are  perfectly  familiar  with  the 
normal  beating.  The  orderly  sequence  of  muscle  movements, 
which  constitute  the  normal  heart  cycle,  is  propagated,  as 
I  have  already  stated,  from  a  single  impulse  born  in  the 
sino-auricular  node.  The  contraction,  starting  from  the 
mouth  of  the  superior  vena  cava,  travels  rapidly  through 
the  auricle,  reaches  the  auriculo-ventricular  node  and 
traverses  this  node  and  the  bundle  which  is  its  continuation  ; 
it  is  distributed  in  an  orderly  manner  amongst  the  mass  of 
ventricular  fibres  in  which  it  ends.  The  normal  rhythm  of 
the  heart  consists  of  a  regular  sequence  of  such  beats,  so  that 
auricle  and  ventricle  contract  in  proper  time  relation  to  each 
other.  Each  stimulus  elaborated  at  the  sino-auricular  node 
requires  a  certain  time  of  preparation,  and  this  time  of 
preparation  is  very  constant  in  given  circumstances.  It  is 
relatively  long,  reaching  nearly  two-thirds  of  a  second  when 


42.  Chapter    I  V. 

the  heart  is  beating  at  a  normal  rate.  Indeed  it  is  the  time- 
of  impulse  preparation  which  controls  the  rate  of  a  normally 
beating  heart.  A  second  characteristic  of  physiological' 
impulses  is  regular  repetition.  Each  impulse  belongs  to  a 
regular  or  rhj^thmic  series. 

The  premature  contraction  or  extrasystole  differs  from 
the  physiological  beat  in  two  fundamental  respects.  Firstly, 
the  impulse  which  gives  rise  to  it  appears  to  require  little 
or  no  time  for  preparation.  It  is  to  this  quality  that  the- 
jDathological  contraction  owes  its  prematurity.  Secondly,  the 
pathological  impulse  is  not  necessarily  one  of  a  rhythmic- 
series,  and  upon  this  character  the  usual  isolation  of  the 
pathological  contraction  depends.  Premature  contractions- 
originate  abruptly  and  may  spring  from  the  auricle,  from  the 
ventricle,  or  from  the  tissues  which  unite  these  tw^o  contractile 
structures.  For  ordinary  chnical  purposes  it  suffices  at  the 
most,  if  we  remember  the  two  chief  classes  of  premature 
beat,  the  auricular  and  the  ventricular. 

If,  while  the  heart  chambers  are  beating  in  a  normal  and 
sequential  manner,  a  pathological  impulse  arises  in  the 
ventricle,  the  ventricular  beat  which  it  awakens  disturbs  this 
rhythm  by  anticipating  the  next  rhythmic  beat,  whence 
comes  the  term  "  premature  contraction."  It  disturbs  the 
sequence  of  ventricular  contractions  in  a  definite  manner. 
Excepting  the  premature  impulse,  the  ventricle  is  dependent 
for  its  stimuli  upon  the  impulses  which  descend  to  it  from  the 
auricle.  Consequently,  after  the  disturbance  produced  by  a 
single  premature  beat,  the  ventricle  rests  until  a  rhythmic 
auricular  impulse  reaches  it.  If  the  accompanpng  diagram 
(Fig.  22)  is  studied,  it  will  be  seen  that  for  the  first  three 
cycles  the  ventricle  follows  the  auricle  in  contraction  ;     a 


Premature  Contractions.  43 

premature  beat  {p)  is  then  interposed  and  as  a  consequence  the 
oncoming  auricular  impulse,  represented  by  the  broken  line, 
arrives  while  the  ventricle  is  already  in  a  state  of  contraction. 
Being  in  contraction,  the  ventricle  shows  no  response,  its 
muscle  is  in  the  "  refractory  "  state.  The  dominance  of 
auricular  impulses  is  reasserted  during  the  succeeding  cycle. 
Thus,  the  original  sequence  is  restored  by  the  fundamental 
heart  rhythm  which  proceeds,  unheedful  of  the  disturbance. 
The  ventricular  contractions,  subsequent  to  the  disturbance, 


Fig.  22.  The  disturbance  produced  by  a  premature  ventricular  contraction 
{p)  is  represented  diagrammatically.  The  auricle  beats  regularly 
throughout.  The  ventricle  responds  to  six  auricular  impulses.  The 
impulse  of  the  central  auricular  systole  is  ineffectual,  for  it  falls  while  the 
ventricle  is  in  premature  systole.  The  abnormal  origin  of  the  ventricular 
beat  is  indicated  by  the  break  in  its  centre.  Note  the  equality  in  the 
lengths  of  periods  a  and  h.     c  is  the  compensatory  pause. 

fall  at  points  which  may  be  accuratel}^  anticipated  ;  the 
period  of  the  disturbance  (6)  is  exactly  equivalent  to  the 
length  of  two  complete  cycles  of  the  normal  rhythm  (a).  The 
diastole  which  follows  the  premature  ventricular  beat  is  long  ; 
the  ventricle  is  waiting.  The  length  of  this  diastole  (c)  is  such 
as  to  compensate  for  the  brevity  of  the  diastole  which 
precedes  it ;  consequently  it  has  been  termed  the  "  com- 
pensatory pause." 

When    a   premature   impulse    originates   in   the    auricle 
the    events    are    somewhat    different.     The    premature    con- 


44  Chapter  I  V. 

traction  of  the  auricle,  which  it  calls  forth,  is  followed  by  a 
similar  and  parallel  disturbance  in  the  ventricle  (Fig.  23),  for 
the  ventricle  responds  to  each  auricular  contraction,  normal 
or  abnormal.  In  all  but  exceptional  instances,  too,  there 
is  a  disturbance  of  the  fundamental  heart  rhythm  :  the 
premature  contraction  {p)  is  followed  by  a  long  pause,  but 
.the  whole  period  of  the  disturbance  (6)  is  not  equivalent,  as 
in  the  case  of  the  premature  ventricular  beat,  to  two  full 
cycles  of  the  normal  rhythm  (a).  The  original  sequence  is 
not  restored. 

~  b 

Fig  23.  A  pi'emature  auricular  contraction  is  represented  diagraminiatically. 
The  auricular  rhythm  is  disturbed  by  the  abnormal  auricular  beat  (p)  ; 
the  disturbance  in  the  ventricular  rhythm  is  parallel,  for  each  auricular 
systole  yields  a  ventricular  response.  The  rhythm  of  the  whole  heart  is 
dislocated,  the  period  a  is  longer  than  the  period  b. 


Etiological  and  pathological  relations. 

Age  and  sex.  Premature  beats  have  been  recorded  at  all 
ages  from  a  few  weeks  to  old  age.  During  the  first  decade 
they  are  rare.  Their  incidence  in  an  age  table  is  actually 
heaviest  between  50  and  70  years  ;  if  the  age  distribution  of 
the  populace  is  considered  in  conjunction  with  this  fact,  it 
becomes  evident  that  they  are  essentially  connected  with 
advancing  years. 

Premature  contractions  are  twice  as  common  in  men 
as  in  women. 


Premature  Contractions.  45 

Associated  conditions  and  provocative  factors.  It  should 
be  remembered  that  any  statistics  compiled  to  show  the 
relations  of  premature  contractions  to  associated  conditions 
and  infections  suffer  from  a  defect.  Those  cases  which  exhibit 
frequent  and  persistent  premature  beats  preponderate  in 
the  tables  ;  for  in  these  circumstances  they  are  conspicuous, 
while  if  they  are  scarcer  they  often  fail  to  attract  attention. 
It  is  probable  that  the  majority  of  people  who  live  to  middle 
life  or  advanced  years  are  affected  in  this  manner  at  some 
time  or  other.  Amongst  patients  who  attend  out-patient 
departments  or  are  admitted  to  the  wards  of  general  hospitals, 
frequent  and  persistent  premature  contractions  are  most 
common  in  those  who  exhibit  definite  symptoms  and  signs 
of  cardiac  disease.  They  are  often  found  in  association  with 
aortic  incompetence  and  mitral  stenosis  ;  an  even  larger 
number  of  curves  is  collected  from  patients  who  present 
signs  of  degenerate  heart  muscle,  as  evidenced  by  enlargement 
and  symptoms  of  muscle  insufficiency  in  the  absence  of  gross 
valve  lesions.  In  yet  another,  and  by  far  the  largest  group 
of  patients,  no  evidence  of  impairment  of  the  heart,  leaving 
the  irregularity  out  of  consideration,  can  be  discovered, 

Extrasystoles  are  not  uncommon  accompaniments  of 
infectious  disease  ;  thus,  in  scarlet  fever  and  diphtheria  they 
may  cause  irregularity  of  the  child's  pulse,  and  local  pus 
infections  are  not  infrequent  associations. 

Of  the  factors  which  appear  to  be  predominantly 
associated  with  them,  gross  lesions  of  the  heart  stand  first. 
Otherwise  an  inquiry  into  the  habits,  history  and  state  of  the 
patient  throws  but  an  obscure  hght  upon  the  causation.  A 
history  of  rheumatic  infection  is  certainly  common  ;  it  was 
present  in  one-third  of  the  cases  in  the  following  series.     In 


46 


Chapter   I  V. 


Premature  nurlcidar  contractions. 


Cardiac  group. 

Myocardial  degeiieriition 
Mitral  stenosis 
Aortic  stenosis 


Remainder. 

Bronchitis  and  emphj'sema. 

Pulmonarj'  tuberculosis 

Dyspepsia 

Lumbago 

Exophtlialmic  goitre.  . 

Api)arently  liealthj^  otherwise 


19 


Premature  ventricular  contractions. 


Cardiac  group. 

Myocardial  Degeneration   . 

24 

Aortic  disease 

12 

Mitral  stenosis 

13 

Angina  pectoris 

/ 

Bright's  disease  and  granu 

lar  kidnej" 

5 

Arteriosclerosis 

:3 

Acute  endocarditis  .  . 

2 

Aneurism 

1 

Remainder. 


Tuberculosis  (lungs  &  pleura 

Bronchitis  and  emphysema 

Gallstones 

Gangrene  of  toes  (senile) 

Epilepsy 

Lifjoma  of  neck 

Fractiu-ed  skull 

Abdominal  tumour    .  . 

Exophthalmic  goitre .  . 

Gastric  ulcer   .  . 

Dyspepsia 

Apparently  healthy  otherwise 


67 


II 


I 
I 
1 
1 
1 
1 
1 
1 
1 
8 

24 


young  adults  excessive  tobacco  smoking  is  recognised  as  an 
exciting  cause  of  their  appearance.  Digitalis  and  its  allies  are 
not  uncommonly  responsible,  when  the  patient  is  under  the 
full  influence  of  these  drugs.  There  are  also  clinical  associa- 
tions between  premature  contractions,  raised  arterial  pressure 
and  digestive  disturbances,  but  these  are  not  fully  understood. 
Many  things  affect  the  frequency  of  premature  con- 
tractions. Fatigue,  subsequent  to  exertion,  is  provocative 
in  all  who  are  predisposed.  The  influence  of  heart  rate 
is  especially  noteworthy.  Hearts  beating  at  100  per  minute 
and  over  are  not  often  disturbed,  and  premature  contractions 
are  very  rare  when  the  heart  rate  exceeds  120.  Fever 
usually  rids  the  pulse  of  this  form  of  irregularity,  and  so 
also  does  any  cause  which  notably  accelerates  the  pulse 
rate.  Thus  they  are  abohshed  during  exercise  and  for  a 
short  period  afterwards,  but  during  the  period  of  slow  heart 


Premature  Contractions.  47 

miction  which  often  follows  exercise,  they  are  frequent  in  the 
predisposed.  As  we  shall  subsec|uently  see,  this  knowledge 
may  often  be  used  advantageously  to  induce  premature  beats 
in  patients  predisposed  to  them.  Suspension  of  respiration 
ior  a  period  compatible  with  comfort  often  suffices.  The 
pathological  beats  are  in  evidence  either  in  the  apnoeic  stage 
or  shortly  after  the  resumption  of  respiration.  Posture  is 
•often  a  potent  factor.  Patients  who  exhibit  numerous 
premature  contractions  while  standing  may  soon  lose  them 
in  recumbency,  and  this  happens  despite  a  slight  decrease 
•of  heart  rate  in  the  last  position.  In  other  patients,  pressure 
upon  the  abdomen  may  abolish  them. 

Observations  go  to  show  that  extrasystoles  are  not 
•caused  by  nervous  impulses  playing  upon  a  healthy  organ  ; 
but  it  seems  to  be  true  that,  if  the  heart  manifests  extra- 
systoles  from  time  to  time,  nervous  impulses,  especially  those 
of  sympathetic  origin,  may  exaggerate  the  tendency. 

The  recognition  of  premature  contractions. 

The  work  accomplished  by  premature  beats  is  small, 
Ibecause  the  periods  of  rest  that  precede  them  are  short. 
"They  may  or  may  not  raise  the  aortic  valves.  Accompanying 
the  "premature  beat,  a  feeble  pulsation  or  a  prolonged  pause 
is  noted  in  the  arterial  pause  ;  auscultation  reveals  early 
first  and  second  sounds  when  the  aortic  valves  are  forced, 
but  only  an  isolated  and  premature  first  sound  if  the  ven- 
tricular pressure  fails  to  top  the  arterial.  The  consequent 
grouping  of  sounds  in  threes  and  fours  is  comprehended  when 
the  nature  and  degree  of  the  corresponding  arrhythmia  are 
<iisGerned,  The  commonest  arrangements  of  pulsations  and 
sounds  are  described  in  the  follomng  paragraphs,  and  are 
illustrated  by  the  accompanying  diagram  and  tracings. 


48 


Chapter    1  V. 


Fig.  24.  A  diagram  showing  common  disturbances  of  the  arterial  pulse  and 
heart  sounds  when  prematiu-e  ventricular  contractions  are  present. 
(a)  Normal  rhythm  ;  (b)  Occasional  premature  beat,  which  affects  arterial 
pressure  ;  (c)  Occasional  premature  beat,  which  fails  to  affect  arterial  passage  ; 
(c/)  Premature  beat  replacing  each  third  normal  beat  and  affecting  arterial 
pressure  ;  (e)  Premature  beat  replacing  each  third  normal  beat  and  failing  to 
affect  the  arterial  jiressure  ;  (/)  Premature  beat  replacing  each  second  normal 
beat  and  affecting  the  arterial  pressure  ;  (.7)  Premature  beat  replacing  each 
second  normal  beat  and  failing  to  affect  arterial  pressure.  The  heart  sounds 
occur  in  groups,  and  the  groups  are  of  four  or  three,  according  as  the  aortic- 
valves  are  raised  or  remain  at  rest  when  the  premature  beat  occurs. 


Premature   Contractions.  40 

In  the  succeeding  paragraphs  I  have  sub-grouped  the 
signs  according  as  the  premature  beat  ("-)  raises  or  {(i)  fails 
to  raise  the  aortic  valves. 

1.  When  a  systole  of  a  regularly  beating  ventricle  is 
replaced  by  a  premature  beat,  this  abnormal  contraction  is 
accompanied  by  an  early  apex  thrust  and  by  (a)  a  weak 
arterial  wave  and  two  extra  sounds,  which,  together  with 
those  of  the  preceding  rhythmic  beat,  form  a  group  of  four 
(Figs.  24  b  and  25)  ;  or  by  {(i)  an  intermission  in  the  arterial 
pulse  and  one  extra  sound,  forming  with  the  sounds  of  the 
preceding  rhythmic  beat  a  group  of  three  (Fig.  24  c). 

2.  When  each  third  beat  of  the  regular  ventricular 
rhythm  is  replaced  by  a  premature  beat,  we  find  a  grouping 
of  the  apex  thrust  in  threes,  of  which  the  third  beat  in  each 
group  is  premature.  The  arterial  beats  («)  are  grouped  in 
threes,*  with  groupings  of  the  apical  sounds,  so  that  two 
normal  heart  sounds  alternate  with  a  group  of  four  sounds. 
(Fig.  24  d)  ;  or  (/5)  are  paired,  with  groupings  of  the  apical 
sounds,  so  that  two  normal  heart  sounds  alternate  with  a 
group  of  three  sounds  (Figs.  24  e  and  30). 

3.  Premature  beats  which  alternate  with  rhythmic 
beats  give  rise  to  pairing  of  the  apical  thrusts  (Figs.  27,  28,  32),, 
and  to  (a)  pairing  of  arterial  beats  of  which  the  second  stroke 
is  weak,  and  to  groupings  of  heart  sounds  in  fours  (Fig.  24  / 
and  29)  ;  or  to  {(i)  halving  of  the  rate  of  the  arterial  pulse, 
and  heart  sounds  in  groups  of  threes  (Figs.  24  g  and  28). 

To  decide  whether  the  premature  beat  arises  in  auricle  or 
ventricle  is  not  usually  possible  without  suitable  recording 
instruments  ;  neither  is  the  differentiation  of  any  great 
clinical  consequence. 

*  Premature  beats  may  also  be  responsible  for  groups  of  three  arterial 
beats  when  they  replace  each  fourth  rhythmic  beat  (Fig.  26). 

E 


50 


Chapter   I  V. 


»<^i^w— l>l   1    ■   W  t  II 


Af>€* 


l^a^Kil 


Fig.   25.     Apex  and  radial  curves,  showing  a  single  premature  ventricular 
contraction.     The  intervals  o  and  b  are  equal. 


RaXL 


Fig.  26.  Radial  curve  and  heart  sounds  in  a  case  in  which  premature 
ventricular  contractions  replace  each  fourth  normal  beat.  The 
preinattire  beats  fail  to  affect  the  pulse. 


tii*'i»iii>viiinTtif»nnnm»iuniniM»»vvnnw>»ivff«a»»  »nm'rr»  rr 


II     B  I      I  il 


if 


B  IB 


Figs.  27  and  28.  Apex  and  radial  curves  and  heart  sounds.  The  normal 
mechanism  passes  into  one  in  which  prematvu-e  ventricular  contractions 
replace  alternate  normal  beats.  Fig.  27  is  from  a  case  in  which  mitral 
regurgitation  was  present.     In  Fig.  28  the  intervals  a  and  b  are  equal. 


/\t>Ok 


Fig.  29.  Premature  ventricular  contractions  replacing  each  second  normal 
beat.  The  heart  sounds  are  grouped  in  fours  ;  the  pulse  is  of  the  form 
termed  pulsus  bigeminus. 


Premature  Contractions.  51 

When  an  occasional  premature  beat  occurs,  the  indica- 
tions of  its  ventricular  origin  are  as  follows  :  {a)  There  is  no 
disturbance  of  the  fundamental  heart  rhythm.  The  presence 
of  this  phenomenon  may  sometimes  be  eUcited,  in  feehng  the 
radial  pulse,  by  anticipating  the  points  at  which  the  rhythmic 
beats,  following  the  disturbance,  ought  to  fall  to  carry  on  the 
original  rhythm  ;  but  it  is  usually  easier  to  detect  disturbance 
of  the  rhythm  than  to  exclude  it  by  this  method.  A  strip 
of  radial  curve  by  itself  is  usually  sufficient  to  distinguish 
one  from  the  other  ;  in  the  instance  of  the  premature  ven- 
triciilar  beat  the  full  period  of  the  disturbance  is  equal  to 
two  normal  cycles  (Fig.  25).  In  the  instance  of  the  premature 
auricular  beat  the  full  period  is  less  (Fig.  31).  (6)  There  is 
often  a  prominent  jerk  and  swelling  of  the  veins  of  the  neck 
(Fig.  30)  at  the  time  of  the  premature  ventricular  beat. 
This  is  brought  about  in  the  following  fashion.  The  ventri- 
cular beat,  falhng  prematurely  as  it  does,  coincides  with  a 
rhythmic  auricular  contraction,  so  that  the  two  heart  chambers 
are  in  systole  together  (see  Fig.  22).  As  a  consequence  of  this 
simultaneous  contraction,  the  auricle  fails,  for  a  single  cycle, 
to  empty  itself  into  the  ventricle,  and  pumps  the  blood  back 
into  the  veins,  (c)  Synchronism  of  the  premature  ventricular 
beat  and  the  rhythmic  auricular  contraction  often  exaggerates 
for  a  cycle  the  corresponding  first  sound. 

When  the  premature  beat  follows  pairs  of  normal  beats  or  alternates 
with  normal  beats,  signs  b  and  c  may  be  present,  but  a  is  usually  valueless 
unless  a  transition  from  a  period  of  disturbance  to  a  period  of  normal  rhythm 
is  graphically  recorded  (as  in  Figs.  28  and  32).  A  comparison  can  then  be 
instituted  between  the  lengths  of  the  disturbed  and  undisturbed  heart  cycles. 
Thus,  in  Fig.  28  the  long  cycles  are  exactly  twice  the  length  of  the  short  ones  ; 
a  is  equal  to  b  ;  premature  contractions  arising  in  the  ventricle  have  created 
an  exact  halving  of  pulse  rate.  In  Fig.  32  the  pause  following  the  premature 
contraction  is  not  compensatory  ;  a  is  longer  than  6  (see  Fig.  23). 

The  effect  of  premature  beats  upon  the  auscultatory 
signs,  when  murmurs  are  present,  are  manifold  ;  yet  most  of 

E  2 


52 


Chapter   I  V. 


Fig.  30.  Curves  from  the  neck  and  radial  artery.  Premature  ventricular 
contractions  replace  each  third  normal  beat,  but  do  not  affect  tlie  pulse. 
An  exaggerated  first  sound  and  a  prominent  wave,  easily  visible  in  the 
neck,  accompanied  each  premature  beat  ;  these  phenomena  result  from 
simultaneous  contraction  of  auricle  and  ventricle. 


Fig.   31.     Apex  and  radial  curves  showing  occasional  premature  auricular 
contractions  ;  a  is  greater  than  b. 


Fig.  32.  A  "  bigeminj'  "  or  coupling  of  heart  beats,  resulting  from  premature 
auricular  contractions,  passing  into  the  normal  rhj^thm  ;  a  is  greater 
than  6 


Fig.  33.  A  bigeminy,  resulting  from  premature  auricular  contractions. 
The  beats  are  paired  in  apical  and  radial  ciu-ves.  Aortic  regurgitation 
was  present. 


Premature  Contractions.  53 

them  can  be  foretold  if  the  general  principles  are  grasped. 
A  systolic  mitral  murmur  will  be  found  with  the  premature 
as  well  as  with  the  rhythmic  beat  (Fig.  27),  but  it  is  usually 
short  and  may  be  absent.  In  aortic  disease,  a  systolic  or 
diastolic  murmur  is  present  at  the  base  of  the  heart  when  the 
premature  beat  raises  the  aortic  valves  (Fig.  33).  On  the  other 
hand,  in  mitral  stenosis,  a  presystolic  mitral  murmur  is  usually 
absent  whether  the  premature  beat  is  auricular  or  ventricular, 
but  in  the  former  instance,  it  is  often  replaced  by  a  presystolic 
sound.  The  absence  of  the  presystolic  murmur  in  the  case 
of  the  auricular  beat  is  attributable  either  to  weakness  of  the 
premature  contraction  or  to  its  coincidence  with  the  preceding 
ventricular  systole. 

More  complex  heart  sounds  are  heard  when  a  premature 
beat  raises  the  pulmonary  but  not  the  aortic  valves,  as 
sometimes  happens  ;  the  second  pulmonary  sound  occurs, 
but  the  second  aortic  sound  is  absent.  This  phenomenon 
has  been  erroneously  ascribed  to  hemisystole,  the  presence 
of  the  second  sound  of  the  right  heart  and  the  absence  of 
that  of  the  left  heart  being  taken  as'  evidences  of  activity 
and  quiescence  of  the  respective  ventricles. 

The   subjective  phenomena   which   accompany  premature 
contractions. 

In  a  very  large  number  of  those  affected,  the  disturbances 
of  heart  rhythm  pass  unnoticed.  On  the  other  hand,  pre- 
mature beats  not  uncommonly  cause  what  patients  term 
"  palpitation."  The  symptom  is  more  prominent  in  young 
subjects,  especially  those  of  female  sex  and  those  afflicted 
by  nervous  instabiUty.  When  numerous,  they  sometimes 
occasion  actual  distress  ;  by  calling  attention  to  the  heart, 


54  Chapter   I  V. 

they  often  induce  anxiety.  The  sensations  experienced  are 
exaggerated  b}^  depression  of  the  general  health,  by  fatigue 
and  by  emotion.  They  are  often  more  noticed  after  the 
patient  retires  for  the  night,  after  excessive  smoking,  after 
a  heavy  meal,  or  after  exertion. 

As  a  general  rule  the  premature  contraction  itself  passes 
unperceived  ;  the  long  pause  which  follows  awakens  a  sense 
of  uneasiness  or  oppression  in  the  chest,  or  a  feehng  of 
void,  while  the  succeeding  contraction  of  the  heart  is 
accompanied  by  consciousness  of  shock  to  the  chest  wall  and 
frequently  by  fullness  or  gripping  in  the  throat.  Patients  in 
whom  these  sensations  are  vivid  sometimes  swaUow,  cough,  or 
inspire  as  soon  as  they  experience  them.  When  a  number  of 
premature  beats  succeed  each  other  at  short  intervals,  and 
consciousness  of  them  is  marked,  anxiety  may  be  profound, 
and  faintness,  coldness  of  the  extremities  and  even  sweating 
may  result. 

The  prognosis  and  treatment. 
It  should  be  clearly  understood  that,  in  speaking  of  the 
prognostic  value  of  premature  beats,  I  speak  of  these  beats 
without  reference  to  the  conditions  with  which  they  are 
associated.  That  when  frequent  and  persistent  they  often 
accompany  grave  affections  of  the  heart  will  be  evident  from 
a  study  of  the  tables  already  given  ;  but  this  fact  does  not 
affect  the  question  discussed*  The  associated  lesions 
give  prognostic  indications  of  their  own  ;  our  inquiries  are 
as  to  whether  a  heart,  which  presents  no  other  sign,  can 
be  regarded  as  healthy  and  as  to  whether,  in  the  case  of  an 
unhealthy  heart,  the  prospect  has  an  added  gloom. 

*  Some  fail  to  grasp  this  point,  and  I  would  enforce  it  by  a  simple  illustra- 
tion. Scars  on  the  tongue  of  an  epileptic  do  not  influence  the  prognosis  of 
the  disease. 


Premature  Contractions.  55 

It  must  be  admitted  that  all  such  beats  are  evidence 
of  a  pathological  condition  and  that  the  pathological  pro- 
cess has  its  seat  in  the  tissues  of  the  heart.  The  presence 
of  premature  contractions  is  an  indication  of  disturbance  of 
cardiac  nutrition,  whether  temporary  or  permanent,  but  it  is 
an  aspect  that  should  not  be  allowed  undue  prominence. 
Very  many  people  are  temporarily  affected  by  premature 
beats  which  do  not  reappear,  while  the  heart  manifests  no 
sign  of  further  damage,  either  at  the  time  or  afterwards. 
In  such  instances  it  is  impossible  to  suppose  that  the 
disturbance  of  the  cardiac  function  has  been  more  than 
transient  or  that  the  nature  of  it  has  been  serious.  Observa- 
tions and  inquiry  also  teach  that  they  may  be  present  con- 
stantly and  for  long  periods,  and  that  those  who  manifest 
them  may  do  so  from  an  early  to  a  good  old  age,  such  patients 
never  showing  any  other  sign  or  symptom  of  cardiac  disability. 
It  may  be  said,  therefore,  that  in  themselves  premature  beats 
cannot  be  regarded  as  evidences  of  serious  involvement  of  the 
heart  muscle,  although  such  involvement  is  often  found  in 
conjunction  with  them. 

The  question  can  be  regarded  from  another  standpoint. 
The  premature  contraction,  when  present  and  frequent, 
inevitably  increase  the  work  of  the  heart,  but  the  amount  of 
the  added  burden  is  not  easy  to  ascertain.  It  is  probably 
not  weighty,  for  where  the  muscle  is  evidently  compromised 
and  frequent  premature  contractions  occur  periodically,  httle 
change  in  the  condition  of  the  patient  can  be  detected  from 
time  to  time,  and  serious  embarrassment  of  the  circulation  as  a 
direct  result  of  them  is  only  suspected  on  rare  occasions. 

Because  they  frequently  consort  with  relatively  grave 
cardiac  maladies,  their  detection  demands  a  close  scrutiny  of 


56  Chapter   I  V. 

the  heart  from  other  points  of  view.  When  after  such 
scrutiny,  no  further  symptoms  or  signs  attributable  to  the 
heart  are  detected,  they  may  be  neglected  in  the  prognosis. 
It  is  also  to  be  observed  that  if  additional  and  significant 
symptoms  or  signs  are  found,  the  prognosis  should  be  based 
on  these,  the  extrasystoles  again  become  neghgible.  In  other 
words,  the}^  serve  a  purpose  in  diagnosis  by  directing  atten- 
tion to  the  heart,  but  are  of  little  or  no  value  in  prognosis. 

I  may  summarise  in  the  statement  that  premature 
contractions  have  a  relatively  insignificant  import,  as  com- 
pared to  many  forms  of  cardiac  irregularity. 

Their  detection  should  not  be  allowed  to  cripple  or  hamper 
the  patient  who  is  the  subject  of  them. 

The  first  standpoint  of  treatment  is  already  indicated. 
The  presence  of  premature  beats  does  not  call  for  a  limitation 
of  bodily  exercise  ;  it  should  not  prejudice  the  vocation  or 
pastime  of  the  patient.  Restrictions  are  necessitated  only 
where  other  signs  render  them  advisable,  or  where  some 
particular  act  or  occupation  is  definitely  known  to  originate 
symptoms  of  a  distressful  land.  The  anxiety  to  which  the 
beats  conduce  in  some  subjects  ma}^  be  materially  allayed  by 
reassurance.  No  drugs  are  known  which  influence  their 
prevalence  ;  digitalis  as  a  direct  measure  is  contra-indicated. 
The  symptoms  are  usually  masked  or  considerably  modified 
by  the  bromides  administered  in  doses  of  from  fifteen  to 
thirty  grains  or  more  a  day  ;  and  these  drugs  are  especially 
useful  in  tiding  a  nervous  or  excitable  j^atient  over  a  jDeriod 
of   disturbance. 

In  patients  who  complain  of  these  beats  and  of  this  alone, 
the  most  suitable  line  of  treatment  is  attention  to  general 
hygiene  and  to  that  of  the  gastro -intestinal  tract  in  jDarticular. 


(     57     ) 

Chapter  V. 

SIMPLE  PAROXYSMAL  TACHYCARDIA. 

Definition. 

Paroxysmal  tachycardia  is  a  term  which  has  been  and 
still  is  applied  to  several  distinct  phenomena.  It  will  be  of 
material  assistance  if  I  restrict  my  description  to  the  simple 
form  and  define  it  as  a  condition  in  which  from  time  to  time 
the  normal  mechanism  is  interrupted  by  a  series  of  rapid  and 
regular  beats,  varying  in  rate  between  100  and  220  per 
minute,*  the  series  starting  and  ending  quite  abruptly. 

The  nature  of  simple  paroxysmal  tachycardia. 

It  has  been  said  that  the  normal  pacemaker  of  the  heart 
lies  at  the  union  of  the  superior  cava  and  right  auricle.  The 
usual  rate  at  which  the  rhythmic  impulses  proceed  from  this 
focus  is  about  72  per  minute  in  the  adult.  If  a  new  centre  of 
impulse  formation  develops  in  any  portion  of  the  heart  wall, 
and  this  centre  forces  responses  at  a  rate  surpassing  that 
of  the  normal  rhythm,  then,  while  it  is  active,  the  new 
centre  dominates  the  movements  of  the  whole  heart.  Such 
are  the  paroxysms  which  we  are  about  to  study  ;  they  consist 
of  sudden  accelerations  of  heart  rate  in  response  to  new 
and  pathological  impulses.     The  paroxysms  may  be  regarded 

*  In  so  defining  it  I  have  pixrposely  excluded  all  accelerations  of  normal 
or  sinus  rhythm,  for  these  are  dependent  upon  altered  innervation.  I  have 
also  excluded  two  forms  of  tachycardia,  which  are  related  to  that  described 
in  the  present  chapter  ;  one,  which  is  regular,  but  in  which  the  aiu'icular 
rate  exceeds  220  per  minute  (see  Chapter  VI)  ;  the  other,  which  is  irregular 
(see  Chapter  VII). 


58  Chapter    V. 

both  clinically  and  pathologically  as  formed  essentially  of 
a  regular  series  of  extrasystoles.  The  new  impulses  are 
elaborated  in  a  single  focus,  whence  the  regularity  of  the 
series,  and  this  focus  lies,  usually  or  always,  at  a  point 
which  is  removed  from  the  pacemaker.*  Fig.  34  opens  with 
three  normal  heart  beats,  and  the  fourth  auricular  contraction 
{jp)  is  premature.     Up  to  this  point  the  diagram  is  identical 


Fig.  34.  A  diagrammatic  representation  of  a  short  paroxysm  of  tachycardia 
arising  in  the  auricle.  The  abnormal  auricular  beats  are  broken  in  their 
centres.  Each  yields  a  ventricular  response.  The  first  abnormal  beat 
occupies  the  same  position  in  relation  to  preceding  events  as  does  that  of 
Fig.  23.     The  short  paroxysm  ends  in  a  cycle  y.     y  is  longer  than  x. 

with  that  shown  in  Fig.  23"|'  ;  it  differs  from  the  earlier  picture 
in  the  repetition  of  the  abnormal  contraction,  five  such  beats 
following  each  other  in  rapid  and  regular  succession.  In  each 
instance  the  ventricle  responds.  The  paroxysm  terminates, 
and  its  end  is  marked  by  a  cycle  {y)  which  is  longer  than  the 
normal  cycle  {x)\\  the  pause  which  follows  a  paroxysm 
derived  from  the  auricle  has  generally  the  same  length  as  that 
which  in  the  same  case  succeeds  an  isolated  premature 
contraction  (see  Fig.  23). 

*  A  statement  which  is  based  upon  electro -cardiography. 

t  In  both  diagrams  I  have  broken  the  auricular  rectangle,  to  emphasise 
the  abnormal  birthplace  of  the  pathological  contractions. 

{  The  interval  {x)  has  been  deliberately  chosen  at  the  onset  of  the 
paroxysm,  because  the  restored  rhythm  of  the  old  pacemaker  is  often  slow 
for  a  few  cycles.  For  simplicity  this  retardation  is  not  figured,  but  it  will  be 
referred  to  ajrain  at  a  later  stace. 


Simple  Paroxysmal  Tachycardia.  69 

How  important  a  clear  conception  of  this  disturbance 
is  will  be  evident,  for  the  nerve  control  of  a  new  centre  of 
impulse  formation  is  not  known  from  analogy  ;  as  a  matter 
of  fact,  the  new  rhythms  show  only  limited  subordination  to 
vagal  and  sympathetic  control. 

The  sites  in  which  the  new  rhythms  develop  are 
numerous  ;  the  abnormal  focus  is  generally  seated  in  the 
auricle,  and  the  usual  sequence  of  contraction  is  consequently 
maintained  in  the  heart  chambers  ;  but  it  may  be  ventricular, 
and  the  auricle  then  responds  reversely  to  the  ventricular 
beats.  The  chief  features  of  the  mechanism  will  be  sufficiently 
impressed  by  a  closer  examination  of  the  commoner  auricular 
variety.  The  diagram  exhibits  a  paroxysm  of  five  beats  ; 
this  short  series  displays  both  onset  and  offset.  Actually 
the  attack  may  last  a  few  seconds  or  a  week  or  more  ; 
whatever  its  length  the  mechanism  is  constant,  but  the 
symptoms  vary  with  the  duration. 

The  extreme  ranges  of  rate  in  this  the  simple  form  of 
paroxysmal  tachycardia  are  from  110  to  220  per  minute  ; 
during  most  paroxysms  the  heart  contracts  160  to  200  times 
per  minute. 

Etiological  and  pathological  relations. 

Age  and  sex.  Paroxysmal  tachycardia  may  occur  at 
any  period  from  childhood  to  old  age. 

Instances  have  been  recorded  in  quite  young  children  ; 
but  these  are  rare.  The  highest  incidence  is  between  the 
ages  of  20  and  30. 

The  disorder  is  a  good  deal  more  frequent  in  men  than 
in   women. 

Heredity  has  been  blamed,  but  the  evidence  is  insufficient 
to  show  that  it  has  any  direct  influence. 


60 


Chapter    V. 


Relations  to  infective  disease.  In  quite  half  the  cases  no 
history  of  previous  illness,  other  than  perhaps  children's 
ailments,  can  be  traced.  Rheumatic  fever  is  the  only  infec- 
tion which  is  at  all  common.  Occasional  instances  appear  to 
have  followed  immediately  upon  malaria,  measles,  pneumonia 
and  scarlet  fever  ;  a  few  of  the  patients  have  been  syphilitic. 

Associated  conditions.  Most  cases  of  paroxysmal  tachy- 
cardia show  no  sign  of  valve  lesion,  and  in  a  large  number 
of  the  patients  there  is  little  or  no  evidence  of  dilatation 
during  the  intervals  between  the  paroxysms. 

Nevertheless,  many  of  them  exhibit  a  limited  field  of 
cardiac  response  and  become  breathless  with  shght  exertion. 
Taking  enlargement,  in  the  absence  of  valve  lesion,  undue 
breathlessness  upon  exertion  and  the  subsequent  development 
of  more  serious  signs  of  cardiac  failure  as  evidences  of  de- 
generation of  the  mycardium,  I  have  placed  ten  of  the 
patients  in  a  corresponding  group  in  the  accompanying 
table.  The  only  valve  lesion  which  figures  prominently  is 
mitral  stenosis,  being  present  in  ten  of  the  cases. 


Paroxysmal  tachycardia  and  associated  conditions 
Mitral  stenosis 
Myocardial  degeneration 
Arterial  disease  (with  and  without  angina) 
Aneurism  (thoracic) 
Renal  disease  and  cardiac  enlargement 
Early  pulmonary  tuberculosis 
No  other  sisns    .  . 


10 
10 
4 
1 
3 
1 
16 

45 


Factors  promoting  attacks.  Exertion  or  emotional  dis- 
turbance chiefly  excite  attacks  in  those  predisposed  to 
them,  and  the  proportion  of  cases  in  which  the  history 
teUs  of  paroxysms  provoked  in  these  ways  is  remarkably  high. 


Simple  Paroxysmal   Tachycardia.  61 

Flatulence,  other  digestive  disturbances,  and  especially  the 
assumption  of  certain  postures,  are  also  provocative  agents. 
The  induction  of  a  first  attack  by  unaccustomed  effort  is 
often  responsible  for  their  hasty  assignment  to  overstrain, 
but  strain  is  never  the  complete  story  ;  probably  damaged 
or  ill-nourished  muscle  is  in  all  cases  the  underlying  mischief. 
Morbid  anatomy.  In  the  instances  in  which  examination 
has  been  possible  after  death,  the  most  prominent  and 
frequent  lesions  have  been  in  the  walls  of  the  heart.  Fibrosis, 
pallor,  friability,  atrophy  and  interferences  with  the  arterial 
supply  are  the  chief  naked  eye  changes  recorded.  In  a  few 
cases  of  tachycardia  nerve  lesions  have  been  found,  but  their 
association  with  the  specific  condition  with  which  we  now 
deal  is  more  than  doubtful. 

The  recognition  of  simple  paroxysmal  tachycardia. 

Whenever  a  patient  is  seen  in  whom  excessively  rapid 
heart  action  is  a  prominent  sign,  the  nature  of  the  accelera- 
tion should  be  determined  ;  the  tachycardia  may  be  a  simple 
acceleration  of  the  physiological  rhythm  or  it  may  be  a 
pathological  rhythm  ;  in  the  first  case  it  is  not,  in  the  second 
case  it  is  primarily  cardiac  in  origin. 

A  heart  rate  of  180  or  more  in  an  adult  is  usually  the 
result  of  pathological  impulse  formation,  and  especially  is  this 
the  case  where  a  heart  lesion  is  known  to  be  present.  A 
cHnical  sign  of  a  pathological  rhythm,  which  experience 
continues  to  impress  me  as  most  valuable,  is  the  following  : 
the  rate  of  the  ventricular  heating  is  preserved  ivhen  the  patient 
passes  from  the  upright  to  the  recumbent  position  ;  it  is  rarely 
altered  by  more  than  a  few  beats  per  minute  even  when 
a  supine  position  is  maintained  for  considerable  periods  of 


62  Chapter    V. 

time.  A  physical  sign  of  equal  diagnostic  importance  may 
be  noted  at  the  onset  or  ending  of  an  attack,  the  increase 
and  decrease  in  rate  at  these  times  is  absolutely  abrupt.  In 
patients  who  are  conscious  of  the  rapid  heart  action,  but  in 
whom  the  beginning  and  ending  cannot  be  observed,  the 
sudden  changes  can  usually  be  ehcited  by  careful  questioning. 

When  tachycardia  is  due  to  a  rise  in  the  rate  of  the 
physiological  rhythm,  as  in  exophthalmic  goitre,  effort 
syndrome,  etc.,  the  rate  responds  to  posture,  rest  and  other 
factors,  and  usually  in  an  advanced  degree  ;  for  the  rhythm 
is  under  some  measure  of  nerve  control.  In  palpitation, 
which  owes  its  origin  to  quickening  of  the  physiological 
rhythm,  the  rise  of  rate  and  the  subsequent  fall  of  rate  is 
gradual  and  not  abrupt. 

In  paroxysmal  tachycardia  other  physical  signs  may 
be  present,  though  their  significance  is  not  so  great.  A 
prominent  and  palpable  pulsation  in  the  veins  at  the  root  of 
the  neck  is  often  present ;  it  may  be  almost  aneurysmal 
in  force.  The  arterial  pulse  is  frequently  irregular  in 
force,  and  at  the  first  examination  may  give  an  erroneous 
impression  of  an  irregularly  beating  ventricle.  No  obser- 
vations are  more  unreUable  than  counts  of  pulse  rates  taken 
in  the  ordinary  manner  during  the  paroxysms  ;  they  should 
always  be  checked  at  the  apex  beat,  either  by  touch  or  hearing. 
The  heart  sounds  are  tic  tac  in  quahty,  and  murmurs  which 
may  have  been  noticed  on  previous  occasions  usuaUy  dis- 
appear while  the  heart  rate  is  raised.  To  know  this  is  of 
importance  in  mitral  stenosis,  in  which  such  attacks  are 
relatively  common  ;  the  presystohc  murmur  is  abohshed. 
When  a  rough  presystolic  murmur  is  lost  by  a  patient  who 
develops  an  accelerated  and  regular  heart  action,  the  dis- 


Simple  Paroxysmal   Tachycardia.  63 

appearance  of  the  murmur  is  generally  attributable  to  an 
abnormal  rhythm.  In  patients  who  suffer  periodically  from 
tachycardia,  the  presence  of  occasional  premature  beats 
during  the  periods  of  quiesence  is  suggestive  that  the  tachy- 
cardia is  due  to  new  rhythm  production. 


"wnmumm MnjipiiiiiiiiiiiiiiiiiuiiininnniiHiiiimiii wbhiiiiiiiIhiiiiii 


\}uKjKmMmmm4^}us}^^ 


Fig.  35. 


IIIIIIIIII        III!       II       II 

Fig.  36. 


JliWlAiWil/liUAAA/JlAAM 

■  Rtlllll  I  I     «   I     i  III         11 

Fig.  37, 

Figs.  35  to  37.  Three  radial  curves,  taken  from  separate  cases  of  paroxysmal 
tachycardia.  In  Fig.  35  a  short  and  complete  paroxysm  is  shown.  In 
Figs.  36  and  37  the  terminations  of  longer  paroxysms  are  seen.  Note  the 
abrupt  beginning  and  ending  of  the  paroxysms,  the  pauses  in  which  they 
terminate,  the  irregularity  of  the  slow  periods  and  the  regularity  of  the 
fast  periods. 

The  curves  are  illustrated  by  Figs.  35-37.  In  Fig.  35 
the  beginning  and  ending  of  the  period  of  tachycardia,  due  to 
abnormal  impulse  formation  at  a  new  auricular  focus,  is 
shown.     The  slow  periods  to  left  and  right  of  it  are  irregular, 


64  Chapter    V. 

for  premature  contractions  interrupt  them.  The  terminations 
of  two  long  paroxysms  are  shown  in  Figs.  36  and  37.  The 
noteworthy  features  of  such  curves  are  several.  The  changes 
from  the  slow  to  the  fast  and  from  the  fast  to  the  slow 
ventricular  rates  are  quite  abrupt.  Following  each  paroxysm 
is  a  relatively  long  pause,  and  this  forms  the  first  of  a  series  of 
pauses  in  a  period  of  retarded  rate.  The  rate  at  the  actual 
termination  is  usually  slower  than  the  average  rate  during 
the  periods  of  quiesence  ;  quickening,  which  is  best  seen 
in  Fig.  36,  occurs  directly  after  the  termination.  The 
slow  rhythm  is  interrupted  by  occasional  premature  con- 
tractions ;  usually  these  may  be  shown  by  special  methods 
to  arise  from  the  same  point  in  the  heart  as  the  paroxysm. 

Symptomatology  of  paroxysmal  tachycardia. 

Broadly  speaking,  the  less  frequent  the  attacks  the  longer 
do  they  last.  In  a  given  patient  the  duration  of  attacks  is 
fairly  constant,  so  that  the  paroxysms  are  similar  from  time  to 
time.  Patients  exhibiting  paroxysms  of  a  few  seconds'  dura- 
tion are  not  uncommon  ;  attacks  which  last  for  several  hours 
are  the  most  frequent  ;  those  of  a  fortnight's  duration  are 
rare  ;  the  attacks  may  be  of  any  intermediate  length. 
Paroxysms  of  accelerated  heart  action  of  the  form  considered 
in  the  present  chapter,  but  of  longer  duration,  are  unknown 
(see  succeeding  chapter). 

The  symptoms  accompanying  paroxysms  of  tachycardia 
are  variable  both  in  their  nature  and  in  their  degree.  They 
are  intimately  dependent  upon  the  duration  of  the  attack,  the 
heart's  rate  during  it,  and  upon  the  capacity  of  the  heart 
muscle.  Amongst  those  in  whom  the  attacks  are  brief, 
it  is  not  uncommon    to    find    that    a    patient    is    entirely 


S'miple  Paroxysmal   Tachycardia.  65 

oblivious  to  the  rapid  heart  action  when  it  occurs,  and  this 
is  more  especially  the  case  when  the  subject  is  elderly  and  of 
the  phlegmatic  type  ;  or  he  may  be  conscious  of  transient 
attacks  only  when  his  attention  is  specifically  drawn  to 
them  or  to  phenomena  commonly  associated  with  them. 
Paroxysms  lasting  half  an  hour  or  longer  are  almost 
invariably  accompanied  by  symptoms,  and  these  become 
aggravated  as  the  attack  proceeds. 

The  immediate  onset  is  signalled  by  a  sudden  sense  of 
discomfort  in  the  region  of  the  heart,  amounting  to  slight 
or  violent  palpitation.  A  tremor  or  fluttering  in  the  chest 
and  a  beating  in  the  neck  are  common.  General  effects, 
such  as  lassitude,  exhaustion,  coldness  and  sweating  are  also 
amongst  the  early  symptoms.  Later,  flatulence,  salivation, 
nausea  and  vomiting  are  prominent.  These  alimentary 
symptoms  are  common  within  an  hour  or  more  of  the  onset,, 
and,  once  estabhshed,  usually  persist  so  long  as  the  heart 
rate  is  maintained.  They  hasten  the  exhaustion  which  is. 
common  and  conspicuous  in  attacks  of  long  duration.  In 
many  patients  a  number  of  symptoms  which  are  directly 
referable  to  the  heart  are  added.  These  may  be  divided  into 
two  groups.  First,  anginal  symptoms,  varying  in  intensity 
from  slight  precordial  pain  or  a  sense  of  compression  with  skin 
tenderness,  to  violent  and  continuous  pain,  radiating  in  the 
characteristic  fashion  over  the  chest,  into  the  neck,  into 
the  left  arm  or  both  arms  and  into  the  abdomen.  Wide 
areas  of  hyperalgesia,  corresponding  to  the  distribution  of  the 
lower  cervical  and  upper  thoracic  nerve  roots,  are  frequently 
present  and  persist  after  the  attack  has  ceased  ;  they  are 
accompanied  by  tenderness  of  the  tendons  of  the  sterno- 
mastoids  and  of  the  bellies  of  the  deltoid,  pectoral  and  other 


66  Chapter    V. 

muscles.     The  patients  complain  of  constriction  of  the  chest, 

variously  described  as  "  a  band  of  tightness,"  "  a  sensation  of 

gripping  "  or  "  a  difficulty  in  breathing."    The  second  group 

of  symptoms  is  a  sequel  to  embarrassed  emptying  of  the  heart. 

In  a  number  of  patients,  as  the  attack  proceeds,  the  limits  of 

cardiac  dulness  move  steadily  away  from  the  middle  line, 

and  as  pallor,  which  is  often  an  early  symptom,  becomes  more 

marked,  cyanosis  and  general  venous  engorgement  are  added. 

The  veins  swell  progressively  ;  the  eyes  seem  sunken,  dark 

areas  appear  below  them  and  the  patient  becomes  haggard  and 

restless.       The  liver   bulges   downwards,   its   edge   becomes 

palpable  and  may  pass  the  umbihcus  eventually.     Tenderness 

is  experienced  when  the  organ  is  pressed  upon,  and  pulsation 

is  seen  in  it ;  the  abdominal  muscles  assume  an  increased 

rigidity  ;  aching  pain  develops  in  the  epigastrium  and  right 

hypochondrium.     In  more  exceptional  cases,  puffiness  of  the 

ankles  and  face  develops  after  a  long  continued  attack.     A 

cough,  accompanied  by  a  frothy  and  sometimes  blood-stained 

sputum,  is  not  infrequent,  and  signs  of  engorgement  of  the 

lungs  in  the  form  of  sibilant  rhonchi  and  moist  rales  are  found 

at  the  bases.     Collapse  of  the  patient  is  prominent  in  the  latter 

stages.     The  attack  may  terminate  in  progressive  failure, 

delirium,  ascites,  general  anasarca  and  death.     Unexpected 

death  also  ends  the  attack  on  occasion,  but  the  great  majority 

of  the  paroxysms  cease  at  the  abrupt  resumption  of  the 

normal    rhythm.     The    actual    cessation    of    the    attack    is 

marked  by  symptoms  of  its  own,  a  sharp  stabbing  pain  in  the 

chest,  or  one  of  more  forcible  thumps  of  the  heart  ;  but  as  a 

rule  the  patient  speaks  only  of  instant  rehef.     Nothing  is 

more  remarkable  than  the  rapidity  with  which  the  natural 

circulatory  conditions    are  restored  when  the  abrupt  fall  of 


Simple  Paroxysmal   Tachycardia.  67 

pulse  rate  comes.  The  dilatation  of  the  heart  and  the 
accompanying  engorgement  of  the  neck  veins  vanish,  as  it 
were,  by  magic.  The  liver  recedes  beneath  the  ribs,  respiration 
becomes  free,  the  pain  is  subdued  and  the  remaining 
symptoms  subside.  Quantities  of  flatus  and  limpid  urine 
are  often  passed  after  an  attack, 

A  var3dng  degree  of  exhaustion  follows  the  severe 
attack,  the  cough  may  continue  for  a  few  hours  or  days, 
and  skin  and  muscle  tenderness  commonly  persists  for  a  day 

or  two. 

Differential  diagnosis. 

The  diagnosis  of  paroxysmal  tachycardia,  during  an 
attack,  rests  upon  careful  attention  to  the  history  of  the 
patient  and  to  those  physical  signs  and  symptoms  which 
have  been  enumerated  already.  As  a  rule,  there  is  httle 
difficulty.  But  a  number  of  errors  do  occur,  and  the  chief 
of  these  may  be  mentioned  ;  they  mostly  depend  upon  the 
prominence  of  symptoms  which  are  referred  to  other  organs, 
and  consequently  upon  a  hurried  examination  of  the  organ 
at  fault,  or  to  neglect  of  the  heart  because  it  presents  no 
murmurs. 

The  stasis  of  the  lungs,  with  dulness  and  crepitations  at 
the  bases,  has  been  attributed  to  pneumonia.  It  is  an  error 
which  should  not  happen,  for  paroxysms  at  this  stage  are 
always  accompanied  by  signs  of  venous  congestion  in  other 
organs.  When  it  has  occurred,  I  beheve  it  has  been  largely 
attributable  to  under  estimation  of  the  heart  rate,  and  the 
mistake  emphasises  the  rule  that  the  heart  rate  should  be 
taken  from  the  apex  beat  and  not  from  the  wrist. 

Anginal  pain  in  the  abdomen,  or  the  pain  of  an  engorged 
liver,  and  accompanied  by  abdominal  rigidity,  vomiting  and 

F    2 


68  .  Chapter    V. 

signs  of  collai^se,  lias  been  mistaken  for  the  symptom  of  a 
perforated  gastric  ulcer,  and  has  led  to  a  dangerous  and  needless 
laparotomy  on  more  than  one  occasion  to  my  knowledge  ; 
and  this  in  patients  in  whom  cardiac  dilatation,  engorgement 
of  the  veins  and  excessive  heart  acceleration,  were  overlooked 
in  the  absence  of  conpicuons  cyanosis. 

A  large  number  of  cases  are  grouped  under  the  compre- 
hensive term  "  heart  strain,"'  and  this  is  apphed  especially  to 
the  patient  in  whom  the  first  attack  has  been  hastened  by 
effort.  In  my  judgment  there  is  no  sufficient  evidence  that  a 
healthy  heart  is  ever  damaged  by  muscular  exertion,  however 
severe  or  prolonged  that  exertion  may  be.  Patients  who  are 
brought  forward  to  illustrate  heart  strain  are  unrecognised 
examples  of  paroxysmal  tachycardia,  examples  of  heart 
poisoning  from  foci  of  infection  or  examples  of  undetected 
structural  heart  disease,  almost  without  exception.  The 
capacity  of  the  normal  heart  to  withstand  added  strain  is 
enormous.  Is  it  to  be  supposed  that  the  organ  is  so  ill- 
protected  that  it  is  to  be  damaged  by  actions  natural  to  man  ? 
Is  it  not  curious  that  in  the  horse,  the  most  heavily  strained 
beast  of  which  we  have  intimate  knowledge,  chronic  heart 
affections  are  conspicuous  by  their  rarity. 

More  than  one  instance  of  paroxysmal  tachycardia  has 
come  to  my  notice,  in  which  "  acute  cardiac  dilatation  "  has 
sufficed  as  a  diagnosis  in  a  pregnant  w^oman,  suffering  in 
reality  from  a  rheumatic  heart  with  mitral  stenosis.  Dilatation 
of  the  heart,  let  it  be  clearly  understood,  does  not  accelerate 
the  pulse.  I  am  aware  that  a  contrary  belief  is  commonly 
held,  but  it  is  an  erroneous  belief.  When  the  heart  is  dilated 
and  beating  rapidly,  these  two  phenomena  are  either  due  to  a 
single  cause,  or  more  commonly,  the  dilatation  is  the  response 


Simple  Paroxysmal   Tachycardia.  09 

of  an  injured  muscle*  to  the  burden  of  excessive  rate.  A 
rheumatic  history  is  not  uncommon  in  cases  of  paroxysmal 
tachycardia,  and  the  characteristic  murmurs  of  mitral 
stenosis,  when  this  valve  lesion  is  present,  are  usually  masked 
during  the  attack.  A  history  of  rheumatic  fever,  or  a  slight 
systolic  thrill  and  an  accompanjdng  apical  murmur,  may 
suggest  a  more  correct  interpretation  of  the  case. 

The  chief  difficulty  arises,  as  these  instances  illustrate, 
when  a  patient  is  seen  for  the  first  time  in  an  attack,  and  this 
is  especially  so  when  no  clea^r  history  is  obtainable.  When 
a  regular  heart  rate  exceeds  160  per  minute  in  an  adult,  the 
presence  of  a  new  rhythm,  rather  than  acceleration  of  the 
normal  rhythm,  should  always  come  first  to  mind  ;  it  may  be 
suspected  even  at  lower  rates.  The  reaction  of  the  rate  to 
posture  is  important.  It  is  perfectly  true  that  very  high 
pulse  rates  are  met  with  in  exophthalmic  goitre,  in  pulmonary 
tuberculosis,  in  alcoholism  and  other  conditions,  but  the 
presence  of  absence  of  the  diseases  or  intoxication  in  question 
may  usually  be  ascertained  and  the  conditions  differentiated. 
Failing  positive  evidence  from  these  sources,  an  examination 
of  the  heart  rate  in  its  response  to  posture  is  of  service.  In 
the  aforesaid  conditions  a  notable  or  conspicuous  decrease  of 
rate  at  or  shortly  after  the  assumption  of  the  supine  posture 
is  the  rule.  Where  we  deal  with  a  new  rhythm,  posture 
influences  the  rate  inappreciably,  if  at  all  ;  neither  is  it  ajffected 
by  repeated  swallowing  or  the  suspension  of  respiration,  or  by 
the  inhalation  of  amyl  nitrite.  A  persistent  tachycardia  of 
140  or  upwards,  maintained  under  a  variety  of  circumstances, 
is  almost  always  due  to  a  new  and  pathological  heart  rhythm. 

*  A  normal  heart  responds  to  increase  of  rate  by  decreasing  in  size  ;  an 
abnormal  heart  responds  either  by  an  immediate  increase  or,  as  is  more 
frequent,  by  a  temporary  decrease  and  subsequent  increase  in  size. 


70,  Chapter    V. 

Patients  who  are  the  subjects  of  relatively  brief  attacks 
occasionally  seek  ad^dce  during  periods  of  quiescence  on  the 
score  of  attacks  of  faintness,  palpitation,  rapid  heart  action, 
etc..  The  true  nature  of  the  condition  may  be  suspected 
or  proved  by  careful  examination.  The  history  of  the 
sensations  at  the  beginning  and  ending  of  the  attack  are 
then  most  valuable.  The  absence  of  symptoms  or  physical 
signs  of  cardiac  involvement,  and  the  absence  of  occa- 
sional or  frequent  premature  beats,  should  suggest  causes 
other  than  those  which  we  are  considering,  though  these  are 
not  to  be  finally  excluded  on  such  scores.  In  nervous, 
debihtated  or  infected  subjects,  an  increased  force  or  rate 
of  the  normal  action  or  excessive  consciousness  of  the  beat 
are  the  most  probable  explanations.  In  cases  of  paroxysmal 
tachycardia  a  prolonged  examination  of  the  patient  is  some- 
times rewarded  by  the  discovery  of  brief  attacks,  for  the 
patient  so  affected  is  often  the  subject  of  more  attacks  than 
those  of  which  he  is  conscious.  In  all  cases  of  doubt  an  effort 
should  be  made  to  see  the  patient  during  an  attack. 

The  prognosis. 

The  prognosis  contains  one  element  of  uncertainty. 
Death  during  paroxysms  has  occurred,  but  the  overwhelming 
majority  of  the  paroxysms  are  tolerated. 

Speaking  of  individual  attacks,  several  prognostic  aspects 
need  emphasis.  The  symptoms  of  the  patient  are  largely 
governed  by  the  reaction  of  the  nervous  system  ;  nervous 
subjects,  especially  women,  awaken  needless  anxiety.  The 
duration  of  the  observed  paroxysm  and  the  length  of  previous 
seizures  have  to  be  considered.  The  outlook  is  more  ominous 
when,  after  a  continuation  of  several  days,  the  heart  shows 


Simple  Paroxysmal   Tachycardia.  71 

signs  of  progressive  weakening,  manifested  by  steady  increase 
in  its  size  and  by  the  pulmonary  and  hepatic  congestion 
Avliich  supervene.  The  strength  of  the  pulse  is  not  prophetic, 
it  may  be  scarceh'  perceptible  in  repeated  attacks.  The 
gravest  symj)toms  are  those  of  increasing  respiratory 
embarrassment,  consequent  upon  oedema  of  the  lungs,  and 
the  onset  of  dehrium  and  general  anasarca.  Nevertheless, 
it  usually  happens  that  when  embarrassment  is  profound  the 
paroxysm  ends,  and  the  patient  passes  in  a  few  minutes  from 
a  condition  of  acute  distress,  and  seemingly  the  utmost 
gravity,  to  one  of  relative  comfort  and  safety.  Briefly,  so  far 
as  the  individual  attack  is  concerned,  it  is  the  duty  of  the 
medical  attendant  to  maintain  a  confident  attitude  ;  however 
desperate  the  case  may  appear  to  the  uninitiated,  if  its  nature 
is  certainly  known,  an  abrupt  cessation  is  to  be  predicted. 
And  this  prediction  ^\i\\  rarely  fail  to  be  fulfilled  ;  although 
I  have  had  exceptional  opportunities  of  witnessing  these 
attacks,  a  fatal  termination  has  not  come  \Wthin  my  personal 
experience.  The  attack,  except  in  the  very  rarest  instances, 
does  not  last  beyond  10  or  14  days  ;  consequently,  if  the 
nature  of  the  attack  is  recognised,  a  confident  prediction 
to  tins  effect  may  be  made. 

The  prognosis  of  the  malady  as  a  whole  should  be  based 
upon  two  cliief  considerations  ;  first  and  most  important, 
upon  an  estimate  of  the  endurance  of  the  cardiac  muscle,  and 
secondly  upon  the  severity  of  the  trials  through  which  it  has 
to  pass. 

The  estimate  of  the  first  factor  is  formed  from  the 
signs  and  symptoms  between  the  attacks  and  from  the 
patient's  reaction  to  effort.  The  prognosis  in  a  case  of 
paroxysmal  tachj'cardia  is  the   same   as   that  in   a   similar 


72  Chapter    Y. 

case  which  shows  no  attacks,  but  with  the  following 
reservations  : — The  attacks  themselves  indicate  muscle 
damage,  and  the  attacks  are  apt  to  place  the  life  of  the 
patient  temporarily  in  jeopardy.  The  reaction  of  the  heart  to 
the  attacks  is  also  of  importance.  A  healthy  heart  reacts  to 
a  pure  increase  of  rate,  amounting  to  a  doubhng  of  the 
normal  rate,  by  decreasing  in  size,  and  the  circulation  may 
be  maintained  for  long  periods.  A  defective  or  diseased 
muscle  reacts  by  dilating.  The  degree  of  dilatation  and  its 
rate  of  progress  during  the  attack  consequently  gauge  the 
degree  of  muscular  involvement.  In  estimating  the  second 
factor  a  survey  of  the  length  and  frequency  of  the  attacks  and 
the  heart  rate  during  such  attacks  is  involved,  as  they  are 
summed  up  by  observation  and  the  previous  history  ;  but  as 
the  attacks  may  cease  at  any  time  never  to  return,  the 
value  of  these  considerations  in  completing  the  prognosis 
has  its  limitations. 

The  possibiUty  of  death  in  a  seizure  is  an  uncertain  factor  ; 
it  necessitates  caution  in  prognosis  when  the  paroxysms  are 
frequent  and  of  long  duration.  Thus,  although  the  factor  of 
unexpected  death  may  be  neglected  in  the  prognosis  of 
individual  attacks  because  its  occurrence  is  remote,  it  may 
not  be  neglected  entirely  when  the  paroxysms  are  dealt 
wdth  collectively. 

The  prognosis,  where  the  heart  between  the  attacks 
seems  sound,  and  where  the  paroxysms  are  infrequent  and 
of  a  few  hours'  duration,  and  the  rate  not  very  excessive,  is 
very  favourable  ;  with  rare  exceptions  such  paroxj'^sms  do  not 
curtail  life,  and  a  prospect  of  long  years  may  be  spoken  of 
to  young  subjects  without  hesitation.  These  patients  always 
wish  to  know  whether  the}^  will  ever  enjoy  freedom.     They 


Simple  Paroxysmal   Tachycardia.  73 

may  be  told  that,  although  such  freedom  cannot  be  promised, 
the  prospect  of  it  is  fair.  The  prognosis  as  a  whole  starts 
from  this  foundation,  and  as  muscle  or  gross  valve  lesions  are 
more  in  evidence,  as  the  attacks  are  longer  and  more  frequent, 
as  the  heart  acceleration  is  greater,  and  as  the  patient  is 
older,  so  the  outlook  is  naturally  less  hopeful. 

The  treatment. 

The  treatment  of  paroxysmal  tachycardia  may  be 
conveniently  dealt  with  from  two  standpoints  ;  the  manage- 
ment of  the  attacks  themselves,  and  the  care  of  the  patient 
during  the  general  course  of  the  malady. 

Are  we  aware  of  any  remedy  which  will  infallibly  cut 
short  a  paroxysm  of  tachycardia  ?  The  answer  to  this 
question  is  still  in  the  negative.  I  have  frequently  seen 
attacks  of  several  hours'  duration  terminate  shortly  after  the 
administration  of  certain  remedies  or  after  certain  inter- 
ferences. The  patients  who  are  the  subjects  of  them  are  often 
aware  of  and  adopt  certain  curative  measures.  In  some 
instances  the  assumption  of  a  given  posture,  sitting  and 
placing  the  head  between  the  knees,  for  example,  or  lying 
supine,  is  a  certain  remedy.  The  induction  of  vomiting,  the 
xelief  of  flatulence,  or  the  application  of  a  tight  abdominal 
Ibinder  may  be  immediately  and  constantly  efficacious  in 
given  cases.  I  have  seen  the  application  of  an  icebag  to  the 
precordium,  a  remedy  which  always  affords  relief,  speedily 
terminate  attacks.  Similarly,  they  have  ceased  shortly  after 
the  administration  of  a  single  intravenous  injection  of 
digitalin  (1-100  gr.)  or  strophanthin  (1-250  gr.).  Firm  pressure 
upon  one  or  other  vagus  nerve  as  it  lies  in  the  carotid  sheath 
has  been  successful.     But  much  more  often  than  not,  such 


74  Chapter    V. 

remedies  are  \vithout  effect  and  the  treatment  finally  adopted 
becomes  palliative  or  symptomatic.  Rest  is  enjoined,  and 
attention  is  paid  to  the  wishes  of  the  patient  in  respect  of 
posture.  Most  frequently  these  sufferers  prefer  to  lie  well 
supported  with  pillows  ;  sometimes  they  prefer  to  stand. 
The  dietary  should  be  fluid,  bland  and  restricted.  Iced 
water  or  milk  are  well  borne  and  are  often  beneficial. 

Local  applications,  the  icebag,  a  mustard  leaf,  cupping 
over  a  distended  or  pain-giving  organ,  be  it  the  heart  or 
the  hver,  often  afford  relief.  Pain,  if  general,  may  be- 
combated  by  more  general  remedies,  such  as  chloral 
or  morphia  ;  but  these  drugs  are  not  often  needed.  The 
induction  of  sleep  in  long-continued  paroxysms  is  essential,, 
and  fortunately  chloral  and  the  opiates  may  be  employed 
with  safety.  Serious  engorgement  of  the  heart  and  signs- 
of  progressive  lung  oedema  or  grave  venous  stasis  are 
indications  of  venesection.  The  letting  of  8  or  12  oz.  of  blood 
will  be  followed  by  improvement ;  fortunately  the  occasion 
for  this  does  not  often  arise.  Respiratory  embarrassment  is 
reheved  and  sleep  induced  by  the  administration  of  oxygen  ;. 
this  gas  is  best  given  through  a  tight-fitting  mask  which 
covers  the  whole  face,  so  that  high  percentages  are  breathed. 

The  treatment  of  the  malady  as  a  whole  is  largely 
governed  by  the  condition  of  the  heart  between  the  attacks. 
A  searching  inquiry  may  reveal  exciting  causes  of  paroxysms  ; 
often,  sudden  exertion  or  emotion  is  the  chief  provocative, 
so  that  to  change  or  forbid  the  usual  employment  may  be 
imperative.  General  care  of  the  health,  the  cleanHness  of  the 
mouth  and  throat,  the  orderliness  of  the  dietary  and  the 
remedying  of  dyspeptic  troubles  and  constipation  may  ward 
off  the  crises.    The  continued  wearing  of  a  broad  abdominaS 


Simple  Paroxysmal   Tachycardia.  75 

belt,  firmly  applied  before  rising  and  discarded  at  bedtime,  is 
sometimes  accompanied  by  the  happiest  of  results. 

The  paroxysms  themselves  do  not  contra-indicate  the 
careful  administration  of  general  anaesthetics,  should  these 
be  necessar}^ 


(      'G     ) 


CHAPTER    YI. 

AURICULAR   FLUTTER. 

Definition. 
Auricular  flutter  is  a  condition  in  which,  as  has  recently 
been  shown,  the  contraction  wave  follows  a  circular  and  never- 
ending  path  in  the  auricle,  the  circuits  being  completed  at 
a  rate  of  from  240  to  350  per  minute  in  different  subjects. 

The  nature  of  auricular  flutter. 
When  the  heart  beats  normally,  each  beat  starts  in  the 
sino -auricular  node  and  the  contraction  thus  begun  radiates 
in  all  directions  into  the  auricular  muscle,  more  and  more 
of  which  becomes  involved  as  the  wave  spreads,  until  the 
whole  is  in  contraction.  The  contraction  wave  spreads  to 
the  furthest  lying  points  of  muscle,  and,  finding  no  further 
path  open  to  it,  dies  out ;  the  auricle  then  remains  quiescent 
until  a  new  impulse  is  discharged  and  the  events  are  repeated. 
In  recent  experiments,  which  have  elucidated  flutter,  the 
beating  of  the  auricle  is  ordered  on  a  quite  different  and 
wholly  abnormal  plan.  A  single  and  continuous  wave 
circulates  in  the  auricle,  usually  around  the  combined 
mouths  of  the  superior  and  inferior  vena  cava.  Unlike  the 
normal  contraction  wave,  this  wave  is  unidirectional  ;  it 
pursues  its  own  wake  and  passes  back  to  and  over  the  same 
path  again  and  again.  It  gives  rise  to  a  very  rapid  and  weak 
action  of  the  auricle,  the  known  limits  of  the  rate  being  from 
220   to    350   per   minute  ;  otherwise   stated,   each   circuit  is 


Auricular  Flutter.  77 

completed  in  1-220  to  1-350  of  a  minute  ;  the  time  taken  for 
the  completion  of  the  circuit,  which  depends  on  the  length 
of  the  circus  and  the  rate  of  conduction,  governs  the  auricular 
rate.  As  the  wave  is  always  circulating,  the  auricle,  as  a 
whole,  never  enjoys  a  true  diastole;  that  is  to  say,  it  is  never 
at  rest  as  a  whole.  At  each  circuit  the  auricle  sends  an 
impulse  towards  the  ventricle,  which  may  or  may  not  penetrate 
to  it.  One  of  the  most  notable  features  of  flutter,  or  extreme 
acceleration  of  the  auricle,  is  its  almost  invariable  association 
with  heart-block.     Flutter,  so  far  as  we  know,  arises  in^the 


Fig.  38.  A  diagrammatic  representation  of  auricular  flutter.  The  contrac- 
tion wave  in  the  atiricle  is  represented  spirally,  to  indicate  its  continuation 
and  constant  re-entry  of  the  same  path.  The  auriciilar  rate  is  extreme  ; 
the  ventricular  rate  is  also  rapid,  though  in  this  instance  only  half  the 
auricular ;   2  :  1  block  is  present. 

auricle  only,*  and  the  rate  of  the  auricular  contractions  is 
so  great  that  the  ventricle  can  rarely  keep  the  pace.  The 
usual  auricular  rates  are  from  260  to  320  per  minute.  The 
usual  ventricular  rates  are  from  130  to  160,  exactly  half  the 
auricular  ;  for  2  :  1  heart-block  is  generally  present  when  the 
patient  first  comes  under  observation  (Fig.  38).  The  auricles 
are  driven  in  merciless  fashion  and  the  reins  of  control,  the 
inhibitory  nerves,  are  powerless.  The  auricle  has  veritably 
seized  the  bit  with  its  teeth.     The  ventricle,  shielded  from 

*  Ventricular    flutter   is   unknown   clinically ;  it   is   probably   unknown 
because,  continuing,  it  would  kill  the  subject  of  it. 


78  Chapter    VI. 

the  whip  by  the  auriciilo-ventricidar  bundle,  lags  behind. 
2  :  1  heart-block  is  the  rule  ;  but  any  grade  of  block  may  be 
present.  Thus  it  happens  that  while  the  auricle  races  at 
300  per  minute,  the  ventricle  may  beat  at  150  (2  :  1  heart- 
block),  at  a  normal  rate  of  75  (4:1  heart-block),  or  at  30 
to  38  (complete  dissociation).  The  speed  of  the  auricle 
once  set  is  wonderfully  uniform  ;  it  may  vary  but  a  few 
beats  per  minute  over  long  periods  of  time  ;  its  beating  is 
always  regular.  The  responses  of  the  ventricle  are  often 
regular  ;  but  they  may  also  be  irregular,  when  the  impulses 


Fig.  39.  A  similar  representation  of  aiu'icular  flutter  with  irregiilar  response 
of  the  ventricle.  The  irregularity  is  of  such  a  Idnd  that  the  beats  of  the 
ventricle  come  in  groups  which  are  accurately  repeated  from  time  to 
time.     Note  the  changes  in  the  ..4s-  Fs  interval,  and  compare  with  Fig.  11. 

from  the  auricle  are  chosen  at  irregular  intervals  ;  especially 
is  this  so  during  a  transition  from  one  uniform  grade  of 
heart-block  to  another.  But  even  when  the  ventricle  beats 
irregularly,  as  each  of  its  responses  is  to  an  auricular  contrac- 
tion forming  one  of  a  perfectly  regular  series,  the  ventricular 
contractions  lie  in  the  curves  at  definite  points  (Fig.  39), 
which  may  be  prejudged  accurately  if  the  grade  of  block  is 
known.  The  point  at  which  a  ventricular  beat  is  placed  is 
governed  by  laws  described  under  heart-block  in  Chapter  III. 
Attacks  of  flutter  are  sometimes  of  quite  brief  duration  ; 
usually,  and  unhke  simple  paroxysms  of  tachycardia,  they 
last  for  months  or  years. 


Auricular  Flutter.  79 

Etiological  and  pathological  relations. 

Age  arid  sex.  Flutter  is  a  comparatively  rare  condition, 
and  though  it  may  occur  at  any  age  it  is  essentially  associated 
with  advanced  years.  Once  I  have  seen  flutter  in  a  child  of 
nine  months,  and  it  has  been  reported  in  other  children. 

In  my  experience  it  is  four  times  as  common  in  males 
than  in  females. 

Relations  to  infective  disease,  etc..  As  a  general  rule, 
no  previous  infection  can  be  traced.  Rheumatic  fever  or 
syphilis  has  seemed  responsible  in  some  cases,  and  in  others 
there  has  been  an  antecedent  infection  of  the  throat  or 
urinary  tract  or  a  history  of  recurrent  attacks  of  gout. 

Associated  conditions.  Occurring  as  it  does  in  elderly 
•cases,  flutter  is  often  associated  with  arterial  sclerosis  ; 
much  increase  of  the  heart's  dulness  is  uncommon  ;  as  a  rule 
there  are  no  murmurs,  but  any  of  the  valve  lesions  may  be 
discovered.  There  are  nearly  always  some  signs  of  degenera- 
tion of  the  heart  muscle,  as  witnessed  to  by  the  symptoms 
of  the  patient  when  the  heart  beats  at  normal  rates. 

Of  a  special  morbid  anatomy  we  have  no  knowledge. 

The  recognition  of  flutter. 

In  a  number  of  patients  the  presence  of  auricular 
flutter  may  be  recognised  by  ordinary  clinical  means  ;  but  in 
perhaps  a  larger  number  the  diagnosis  is  only  possible  when 
a  special  method  (the  electrocardiographic  particularly)  is 
■employed. 

During  the  2  :  I  heart-block  phase.  When  patients  who 
exhibit  flutter  are  first  seen,  the  rate  of  the  ventricular  action 
is  usually  half  the  auricular.  The  history  often  includes 
palpitation,  whose  onset  was  sudden  months  or  years  before 


80  Chapter    V  I. 

and  was  perhaps  accompanied  by  fainting.  A  regular  and 
persistent  ventricular  action  of  from  130-160  per  minute  in  an 
elderly  subject  is  a  most  suspicious  circumstance,  and  its 
discovery  should  always  be  followed  by  a  special  examination 
for  other  signs  of  flutter.  The  patient  may  give  a  history  of 
short  paroxysms  of  many  years' standing  and  may  speak  of 
this  the  final  attack  which  he  is  unable  to  discard.  If 
tachycardia  persists  for  a  month  or  more  at  one  of  the  stated 
rates,  and  there  is  absolutely  no  change  of  rate  with  change 
of  posture,  rest  or  exercise,  the  condition  is  almost  certainly 
flutter.  A  most  suggestive  incident  is  the  constant  repetition 
of  the  same  high  rate  in  the  pulse  chart,  or  the  finding  of 
exactly  the  same  high  heart  rate  at  intervals  of  weeks  or 
months. 

From  time  to  time,  in  certain  individuals,  and  usually 
during  periods  of  emotion  or  exertion,  the  ventricular  rate 
springs  momentarily  to  the  full  auricular  rate  ;  the  resulting 
disturbance  is  profound,  and  patients  who  retain  consciousness 
subsequently  give  vivid  accounts  of  the  experience  ;  fainting 
is  common  in  flutter  patients. 

Firm  pressure  upon  the  carotid  sheath,  on  left  or  right 
side,  sufficient  to  obliterate  the  vessel  and  stimulate  the  vagus 
nerve,  often  produces  a  conspicuous  slowing  of  the  j)ulse  or  a 
lapse  of  many  beats  (Fig.  40).*  Digitalis,  given  in  full  doses^ 
always  slows  the  pulse  and  creates  irregularity.  The  radial 
curves,  when  the  pulse  is  fast,  often  exhibit  alternation, 
(see  Chapter  VIIT). 

Auricular  flutter,  yielding  a  2 : 1  response  of  the  ventricle^ 
is  the  easiest  form  in  which  it  is  recognisable  ;  fortunately 

*  But  it  leaves   the  auricular  rate  unaltered,  the  vagus  acts   here   by 
preventing  the  auricular  impulses  from  reaching  the  ventricle  (heart-block). 


Auricular  Flutter. 


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Chapter    VI. 


this  is  also  the  most  important  form  in  wiiicli  to  recognise 
it,  for  it  then  requires  and  responds  well  to  treatment. 

If  flutter  occurs,  as  it  may  do,  in  short  paroxysms,  it 
is  apt  to  be  confused  with  simple  paroxysmal  tachycardia, 
for  the  symptoms  are  similar  and  the  signs  are  very  similar. 
Often  they  may  be  differentiated  clinically,  nevertheless. 
Common  ventricular  rates  in  simple  paroxysmal  tachycardia 
are  from  180  to  220  per  minute.  If  the  ventricle  beats 
regularly  at  these  rates,  auricular  flutter  may  be  excluded, 
because  auricular  rates  equalUng  or  surpassing  360  (which  is 


V  /  V  -I 


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Fig.  42.  A  .series  of  three  radial,  curves  from  a  case  of  flutter,  showing  the 
chief  features  of  the  irregularities  produced  by  ruixed  responses.  The 
curves  have  a  superficial  resemblance  to  premature  contractions  ;  but 
that  the  irregularity  is  not  produced  in  this  fashion  is  clearly  indicated 
bj'^  the  manner  in  which  the  curves  "  space."  The  bracketed  portions 
of  each  curve  are  of  equal  dviration,  and  they  are  of  equal  duration  because 
they  correspond  to  equal  numbers  of  auricular  cycles.  The  number  of 
auricular  cycles  to  each  ventricular  cycle  is  marked  above  each  pulse  beat. 

the  double  of  180)  are  unknown.  Actually  the  confusion  is 
not  of  much  consequence,  since  short  attacks  of  flutter 
should  be  treated  as  are  simple  paroxysms  unless  the  symp- 
toms show^  extreme  urgency. 

As  simple  paroxysms  of  tachycardia  do  not  last  more 
than  14  days,  and  as  flutter  usually  lasts  months  or  years, 
they  are  not  usually  confused. 


Auricular  Flutter.  83 

During  the  stage  of  irregular  responses .  If  the  responses 
of  the  ventricle  are  irregular,  a  little  exercise,  often  no  more 
than  raising  a  limb  off  the  bed,  immediately  accelerates  the 
ventricular  action  and  induces  perfect  regularity  of  the  pulse 
(2:1  heart-block)  (thereby  differentiating  the  condition  from 
auricular  fibrillation),  and  this  regular  pulse  action  may  then 
be  tested  in  the  manner  described  in  the  preceding  paragraphs 
(Fig.   41). 

The  character  of  the  radial  curve  gives  an  immediate 
clue  to  the  condition  (Fig.  42  and  explanation). 

When  the  responses  of  the  ventricle  are  infrequent.  It  is 
under  these  circumstances  that  flutter  is  so  difficult  to 
recognise  by  ordinary  clinical  means.  A  patient  may  possess 
a  fluttering  auricle  and  the  pulse  may  be  within  normal  limits 
of  rate  and  may  be  regular.  Fortunately  for  diagnosticians, 
such  cases  are  rare  ;  moreover,  the  failure  to  detect  the 
flutter  at  such  times  is  relatively  of  little  consequence.  In 
some  patients  the  movements  of  the  auricle  are  transmitted 
to  the  veins  of  the  neck  and  may  be  identified  as  very  rapid, 
minute  and  regular  undulations  (Fig.  426). 

The  symptomatology  of  flutter. 

The  symptoms  associated  with  auricular  flutter  need  not 
long  detain  us.  In  patients  in  whom  the  acceleration  occurs 
in  short  paroxysms  the  symptoms  are  identical  with  those 
of  simple  paroxysmal  tachycardia  ;  they  vary  in  intensity 
according  to  the  heart  rate  and  according  to  the  resisting 
power  of  the  ventricular  muscle. 

But  in  patients  who  experience  longer  periods  of  disturbed 
heart  action,  and  these  are  more  frequent,  for  flutter  generally 
persists  for  months  or  years,  the  subjective  sensations  are 


84 


Chapter    VI. 


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Auricular  Flutter. 


85 


modified.  Although  the  reason  is  not  clear,  the  symptoms  of 
flutter  seem  less  profound  than  is  to  be  expected  from  a  study 
of  many  simple  attacks  of  tachycardia.  Thus,  not  infre- 
quently, the  action  of  the  heart  may  be  accelerated  to  130  or 
150  for  periods  of  a  year  or  more,  and  yet  the  symptoms 


Fig.  43.  A  series  of  four  curves,  showing  the  effect  of  cUgitalis  medication 
upon  flutter,  (a)  The  heart  is  beginning  to  respond  to  digitahs  and 
occasional  periods  of  4  :  1  heart-block  are  seen,  interrupting  an  otherwise 
regular  2  :  1  mechanism  ;  the  rate  of  the  auricles  was  264  per  minute*  and 
that  of  the  ventricles  132.  (6)  Further  slowing  a  few  days  later.  The 
beats  of  the  ventricle  now  occur  in  groiips,  or  the  mechanism  is  reduced 
to  a  4  :  1  grade  of  heart-block,  (c)  A  few  days  latet ;  the  ventricle  becomes 
grossly  irregular  with  the  establishment  of  fibrillation.  The  digitalis 
having  been  withdrawn,  the  normal  and  regular  mechanism  is  resumed 
(d)  ;  the  rate  of  the  auricle  and  ventricle  being  now  64  per  minute. 

consist  of  little  more  than  a  sense  of  exhaustion  and  fatigue 
after  exertion.  The  occupations  of  such  patients  are 
limited,  but  signs  of  failure  in  the  form  of  stasis  and  dropsy 
do  not  necessarily  supervene.  I  have  known  a  patient  in 
whom  the  ventricle  has  beaten  at  140  per  minute  night  and 
day  for  seven  vears  ;  his  condition  was  much  the  same  at  the 


S6  Chapter    VI. 

beginning  and  end  of  this  period.  8uch  cases  illustrate  the 
resistance  of  a  tolerably  healthy  heart  to  prolonged  and  con- 
siderable strain  in  a  most  dramatic  manner.  Such  tolerance  is 
to  be  attributed  perhaps  to  the  reserve  power  of  the  ventri- 
cular muscle.  Naturally  there  are  cases  of  flutter  in  which 
signs  of  congestion  are  visible  at  an  early  stage  ;  but  in 
reviewing  a  series  of  cases,  one  cannot  but  be  impressed  by 
the  infrequence  of  these  signs  of  failure,  as  compared  to  their 
relatively  high  incidence  in  simple  paroxysms  of  similar  rate. 
As  I  have  already  indicated,  there  is  an  additional 
sj^mptom  complex  in  flutter  ;  it  results  when  the  ventricle 
assumes  the  full  auricular  rate  ;  an  acceleration  of  the 
ventricle  to  300  per  minute  places  the  hfe  of  the  subject  in 
immediate  jeopardy,  the  symptoms  are  profound  and 
consciousness  is  usually  lost  ;  such  attacks,  being  survived, 
are  necessarily  fleeting. 

The  2J'>'ognosis. 

As  stated,  I  have  known  the  condition  to  last  unin- 
terruptedly' for  seven  years,  the  ventricle  beating  without 
cessation  at  140  per  minute.  How  much  longer  this  high  rate 
may  be  maintained  in  the  presence  of  a  tolerably  efficient 
circulation  cannot  be  stated. 

We  gather  a  general  idea  of  the  prospect  upon  the 
lines  discussed  in  treating  of  the  simple  paroxysms  of  the  last 
chapter.  It  may  be  based  ujDon  a  general  consideration  of 
the  strength  of  the  heart  muscle,  and  of  the  burden  Avhich 
this  muscle  has  to  carr}^  Important  in  this  respect  is  the 
response  to  treatment,  for  most  cases  are  amenable  to 
specific  measures,  as  we  shall  see  in  the  succeeding 
paragraphs. 


Auricular  Flutter.  8.7 


The  treatment. 


The  treatment  of  long  continued  flutter  of  the  auricles  is 
often  conspicuously  successful.  Even  after  the  acceleration 
has  lasted  for  many  months,  or  even  several  years,  the  natural 
rhythm  of  the  heart  may  at  times  be  restored  by  suitable 
medication.  The  remedy  is  digitalis  or  an  allied  drug.  My 
experience  tells  me  that  the  ventricular  rate  can  always  be 
reduced  by  giving  digitalis  or  strophanthus  in  full  doses,  and 
may  be  maintained  at  the  reduced  rate  so  long  as  treatment  is 
continued. 

Further,  I  have  found  that  if,  having  obtained  this 
reaction,  the  dosage  can  be  increased,  the  flutter  ceases  and 
fibrillation  (a  condition  described  in  the  next  chapter)  takes 
its  place  ;  if,  now,  the  remedy  is  withdrawn,  the  fibrillation 
soon  vanishes  in  most  cases  and  the  normal  rhythm  is 
immediately  resumed.  I  have  seen  these  changes  in  a  number 
of  patients  and  can  speak  confidently  of  the  success  of  the 
remedy  in  them.  Occasional  intolerance  to  the  drug,  the 
onset  of  gastro -intestinal  symptoms,  appears  to  the  sole 
limitation  ;  strophanthin  may  then  be  administered  intra- 
venously with  equally  happy  and  much  more  speedy  results. 
It  may  be  asked  if  the  flutter  ever  returns  when  it  has  been 
abolished.  In  one  of  my  cases  it  returned,  but  renewed 
treatment  again  restored  the  normal  rhythm,  and  this  per- 
sisted. The  secret  of  the  treatment  seems  to  lie  in  throwing 
an  obstruction  in  the  path  of  the  circulating  wave ;  digitahs 
may  conceivably  do  this  by  creating  a  region  of  block  in  the 
auricle.  Flutter,  once  it  comes,  establishes  and  maintains 
itself;  it  constitutes  a  really  vicious  circle;  the  same  tendency 
is  found  in  fibrillation,   a   condition  which  we  shall   discuss 


88  Chapter    VI. 

presently.     Being  checked,   the  cause  of  its   persistence  is 
removed. 

When,  in  such  patients  as  have  signs  of  cardiac  failure, 
flutter  is  removed  and  the  normal  rhythm,  with  normal  heart 
rate,  takes  its  place,  the  change  in  the  general  condition  is 
remarkable  and  almost  immediate.  Engorgement  and  dropsy 
rapidly  disappear  ;  breathlessness  and  other  discomforts  are 
relieved  ;  the  customary  occupations  of  life  may  be  resumed. 


(     89     ) 


Chapter   Vll. 

AURICULAR  FIBRILLATION. 

Definition. 

A  condition  in  which  the  auricles  fail  to  contract 
en  masse,  the  muscle  activity  consisting  only  of  fibrillary 
twitchings  ;  the  normal  and  regular  impulses  transmitted  to 
the  ventricle  are  absent,  while  rapid  and  irregular  impulses 
produced  in  the  auricle  replace  them  and  produce  gross 
irregularity  of  the  ventricular  action. 

The  nature  of  auricular  fibrillation. 

When  we  inspect  the  normally  beating  heart  of  an 
animal  the  systoles  of  both  auricle  and  ventricle  are  readily 
discerned.  The  movement  of  the  auricle  is  a  sharp  flick, 
most  clearlj^  perceptible  in  the  length  of  the  auricular 
appendix,  for  in  this  line  the  shortening  is  greatest.  When 
the  auricle  is  forced  into  fibrillation  or  deUrium,  the 
appearances  are  quite  distinctive  ;  the  muscular  walls  are 
maintained  in  a  position  of  diastole  ;  systole,  either  complete 
or  partial,  is  never  accomplished  ;  the  structure  as  a  whole 
rests  almost  immobile  ;  but  close  observation  of  the  muscle 
surface  reveals  its  extreme  and  incessant  activity,  rapid  and 
minute  twitchings  and  undulatory  movements  are  visible 
over  the  whole.  Recent  investigation  points  to  the  nature 
of  the  auricular  disturbance.  It  is  related  to  flutter,  but 
instead  of  the  single  smooth  circulating  wave,  which  produces 


90  Chapter    VII. 

a  regularly  beating  auricle,  the  circulating  wave  or  waves  are 
sinuous,  the  path  varies,  and  the  waves  seemingly  colUde  or 
re-enter  new  channels  where  from  instant  to  instant  they  find 
these  free.  This  mechanism  is  not  easy  to  represent  in  dia- 
grammatic form,  but  I  have  attempted  to  depict  multiple 
and  variable  circulating  waves  in  Fig.  44.  As  in  flutter, 
the  auricle  as  a  whole  is  never  in  a  state  of  diastole;  its  tissues 
have  suffered  functional  fragmentation.  The  precise  manner 
in  which  this  change  comes  is  still  unknown.  When  the 
auricle    is    fibrillating   its    normal,    regular    and    co-ordinate 


Fig.  4:4:.  A  cliagrammatic  representation  of  auricular  fibrillation.  The 
fibres  of  the  auricle  do  not  contract  co-ordinatelj'.  The  contraction  waves, 
which  are  multiple,  follow  varying  and  sinuous  paths,  colliding  with  each 
other  or  re-entering  tracks  through  which  they  or  their  neighbours  have 
previously  passed.  Occasional  impulses  leave  the  auricle  at  irregular 
intervals,  and  many  of  these  proceed  to  the  ventricle  and  stimulate  it. 
Its  action  is  therefore  rapid  and  irregular. 

contractions  are  in  abeyance,  and  consequently  the  ventricle 
is  robbed  of  the  regular  impulses  which  form  its  accustomed 
supply.  These  are  replaced  by  numerous  and  haphazard 
impulses,  escaping  to  the  ventricle  from  the  turmoil  wliich 
prevails  in  the  upper  chamber  ;  the  change  in  the  action  of 
the  ventricle  is  consequently  profound.  Its  rate  of  beating 
rises  considerably,  and  the  contractions  follow  each  other  in  a 
completely  irregular  fashion  (Fig.  44)*. 

*  Ventricular  fibrillation  is  incompatible  with  life.  It  is  probably 
responsible  for  many  instances  of  unexpected  death  ;  this  end  is  more 
especially  suspected  in  certain  cases  of  auricular  fibrillation  and  in  death 
under  chloroform  anaesthesia. 


Auricular  Fibrillation.  91 

Such  are  the  events  in  experiment,  and  those  of  the 
chnical  condition  are  identical,  mth  one  proviso. ;  since  in  the 
experimental  heart  the  tissues  controlHng  the  conduction  of 
impulses  are  healthy,  the  rate  of  the  ventricular  contractions 
is  doubled  or  even  trebled  ;  but  in  the  human  subject,  the 
conducting  tissues  may  be  either  intact  or  damaged  ;  con- 
sequently the  ventricular  rate  varies  widely  in  different 
patients,  according  as  access  to  the  ventricle  is  full  or  limited. 
While  a  free  passage  yields  rates  approaching  200  per  minute, 
damage  to  the  junctional  tissues  may  reduce  the  rate  to  40  or 
less  :  the  usual  rates  lie  between  90  and  140. 

Etiological  and  pathological  relations. 

Age.  While  fibrillation  has  been  observed  from  childhood 
to  old  age,  it  is  extremely  rare  before  the  age  of  17  years.  In 
studying  the  age  distribution,  the  cases  are  conveniently 
divided  into  rheumatic  and  non-rheumatic  groups.  This 
division  clearly  shows  that,  independent  of  rheumatism,  the 
affection  is  related  to  advancing  years  ;  the  highest  incidence 
is  in  the  sixth  and  seventh  decade.  In  the  rheumatic  group, 
the  incidence  is  heaviest  between  the  twentieth  and  thirtieth 
years  ;  it  is  almost  as  heavy  in  the  fourth  and  fifth  decade, 
but  lightens  as  the  years  mount  further. 

Sex.  Auricular  fibrillation  is  much  more  common  in 
men  than  in  women,  but  the  preponderance  in  males  is 
chiefly  in  the  non-rheumatic  group.  -Where  there  is  a 
rheumatic  history  the  sexes  bear  the  burden  more  eq^ually. 
The  relative  frequency  of  fibrillation  in  rheumatic  women 
is  finked  with  the  prevalence  of  mitral  disease  in  this  sex  ; 
mitral  stenosis  and  auricular  fibrillation  are  bosom  com- 
panions. 


92  Chapter    VII. 

Relation  to  infections  ;  associated  conditions.  Amongst 
a  collection  of  152  cases  a  rheumatic  or  choreic  history  was 
found  7 1  times  ;  in  four  instances  at  least  there  was  a  history 
of  one  or  other  affection  in  the  family.  Amongst  the  re- 
mainder, mitral  stenosis  was  present  in  26,  and  pericardial 
adhesions  or  effusion  in  two  cases.  If  these  patients  are 
collected  to  form  a  rheumatic  group,  the  subdivision  includes 
101  cases,  or  66  per  cent.  The  prevalence  of  fibrillation 
amongst  those  who  suffer  from  mitral  constriction  is  especi- 
allj^  noteworthy  ;  79  of  the  cases,  or  52  per  cent.,  had  this 
valve  lesion.  The  relation  to  mitral  stenosis  may  be  traced  in 
another  and  equally  emphatic  manner.  Of  106  cases  of 
mitral  stenosis  collected  in  an  out-patient  department,  22, 
or  approximately  one-fifth,  suffered  from  auricular  fibrillation. 
The  proportion  amongst  in-patients  is  much  higher  ;  it 
exceeds  50  per  cent. 

In  the  table  I  have  classed  a  group  as  myocardial 
degeneration  ;  it  includes  those  in  whom  the  heart  irregu- 
larity was  the  outstanding  feature,  though  many  of  the  cases 
presented  signs  of  cardiac  failure  in  addition  to  the  irregu- 
larity. Aortic  disease,  arterial  disease  and  granular  kidney 
are  the  chief  lesions  in  other  groups.  Of  all  cases  of  cardiac 
failure  admitted  to  a  general  hospital  60  to  70  per  cent, 
manifest  this  disorder  of  the  heart  ;  it  is  difficult,  therefore, 
to  over-emphasise  its  importance. 

Of  etiological  factors,  rheumatism  is  predominant,  as  we 
have  seen  ;  a  history  of  other  infections,  "  influenza  " 
amongst  them,  is  given  by  many  patients,  but  the  influence 
of  these  infections  is  imperfectly  understood. 

An  idea  has  been  prevalent  in  the  past  that  dilatation 
of  the  heart  may  itself  lead  to  gross  irregularity  of  the  organ, 


Auricn lar  Fibrillafion . 


93 


Mitral  stenosis 

51 

Myocardial  degeneration  .  . 

11 

Rheumatic  or         .  Pericardial  adhesions 

1 

-71 

choreic  history     Aortic  disease 

6 

Renal  diseases 

2 

Rheumatism  or     /  Mitral  stenosis 

2 

h 

chorea  in  family  (Myocardial  degeneration  .  . 

2 

/Mitral  stenosis 

19 

\ 

Arterial  disease 

7 

Myocardial  degeneration  .  . 

17 

Renal  disease 

11 

Aortic  disease 

3 

Aneurism     .  . 

2 

. 

Emphysema  and  bronchitis 

2 

No   history   of 
rheumatism  or  . 

Subacute    infective     endo- 
carditis 

2 

)70 

chorea 

Pericardial    adhesions    and 

pericardial  effusion 
Tuberculous  pleurisy 
Syphilitic  heart 
Congenital  heart     .  . 
,  Chronic  alcoholism 

2 

/ 

^  Pneumonia .  . 

^^«"™^tis^^f^  JMitral  stenosis         .. 
chorea  not  noted  J 

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such  as  is  here  described.  This  idea  is  fanciful.  Dilatation 
does  not  produce  irregularity,  but  irregularity,  when  associated 
with  rapid  ventricular  action,  may  dilate  an  injured  ventricle. 


*  The  heavy  figures  mark  the  rheumatic  group. 


94  Chapter    VII. 

Morbid  anatomy.  Tliat  valve  lesions  are  present  in  a 
number  of  the  cases  is  obvious  from  the  bedside  examinations  ; 
enlargement  of  the  whole  heart  is  common,  and  dilatation 
or  hypertrophy  of  the  auricles  is  more  frequent  than  the 
valve  lesions  which  might  be  held  to  account  for  them.  The 
most  constant  structural  alterations  which  are  found  are 
discovered  b}^  histological  examination  of  the  heart  muscu- 
lature. Usually  it  shows  a  more  or  less  intense  grade  of 
subacute  or  chronic  inflammatory  change  progressing  to 
fibrosis,  and  the  auricles  are  conspicuously  affected.  A  diffuse 
fibrosis,  accompanied  by  leucocytic  infiltration  and  atrophy  of 
the  neighbouring  muscle  cells,  is  the  most  frequent  change. 

Such  is  the  tale  told  by  the  microscope,  but  it  does  not 
justify  us  in  holding  that  the  inflammatory  reaction  is  the 
cause-  of  the  disturbance.  We  examine  the  hearts  of  those 
who  die,  and  most  die  with  all  the  classical  signs  of  heart 
failure.  Many  of  the  microscopic  lesions  are  to  be  regarded 
as  the  result  of  infections  producing  heart  failure  rather 
than  fibrillation.  Similar  lesions  are  found  where  fibrillation 
has  never  occurred,  and  hearts  Avhich  have  shown  this 
disorder  may  not  present  the  lesions  described. 

The  recognition  of  auricular  fibrillation. 

Auricular  fibrillation  gives  rise  in  a  chnical  case  to  two 
series  of  phenomena — the  one  dependent  upon  the  virtual 
paralysis  of  the  auricle  ;  the  other  dependent  upon  the 
disordered  action  of  the  ventricle. 

It  will  be  convenient  to  study  the  ventricular  signs 
first.  The  irregularity-  varies  in  form  according  to 
the  rate  of  the  contractions.  When  the  heart  is  beating 
rapidly   at    100-160   per   minute,   the   grade   of    disorder    is 


Auricular  Fibrillation.  9S 

maximal.  The  pulcJe  supplies  indifferent  news  of  the  ventricu- 
lar rate,  many  pulsations  fail  to  reach  it  (such  beats  are 
marked  with  asterisks  in  Fig.  40).  The  pulse  is  a  medley 
of  beats  of  many  sizes  (Fig.  45),  an  intimate  mingling  of 
changing  pauses ;  now  the  beats  are  almost  uniform  in  strength 
and  j)acings  ;  now  feeble  pulsations  chase  along  rapidly  ; 
now  the  pulse  is  lost  ;  now  it  returns  with  increased  vigour. 
Feel  the  pulse  in  such  cases  and  the  nature  of  the  disease  is 
disclosed  ;  the  more  turbulent  the  pulse,  the  more  certain  is 
the  evidence.  It  is  when  the  rate  is  slow  that  close  attention 
and  more  experience  are  often  asked,  for  wHh  slower  rate  the 
disorder  is  less  pronounced  ;  all  the  heart  beats  now  reach  the 
wrist  and  the  irregularity  comprises  minor  variations  in  the 
length  of  diastole  (as  in  Fig.  48)  ;  it  may  then  escape  notice, 
and  a  heedful  examination,  concentrating  upon  its  presence  or 
absence,  alone  brings  it  to  discovery.  Short  pulse  curves 
reveal  the  irregularity  on  all  but  rare  occasions.  The  nature 
of  the  arrhythmia  is  such  that  the  heart  action  is  never  quite 
regular,  and  seldom  do  two  beats  of  a  precisely  similar 
character  or  length  lie  adjacent.  No  tAvo  whole  strips  of  curve 
are  alike  ;  the  cycles  bear  no  simple  length  relation  one  to 
another.  Proportion  between  the  force  of  an  arterial  pulse 
and  the  length  of  rest  preceding  it  is  often  lost  (Figs.  45  and 
46)  ;  a  strong  beat  may  succeed  a  brief  diastole  and  a  weak 
beat  may  succeed  a  long  one.  When  the  pulse  is  slow, 
only  beat  to  beat  measurement  may  disclose  the  irregularity. 
The  fully  developed  disorder  of  the  ventricle  is  readily 
appreciated  at  the  apex.  The  heart  sounds  are  modified  ; 
they  vary  in  intensity  and  the  variation  runs  hand  in  hand 
with  the  strength  of  the  beats.  First  and  second  sounds  are 
present   with    each   systole   which   yields    arterial   pulsation 


96 


Chapter    VII. 


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98  Chapter  VII. 

(Fig.  45)  :  a  first  sound  stands  isolated  when  the  pulse  beat  is 
missing  (Fig.  46).     If  a  systolic  mitral  murmur  is  present,  it 
accompanies  each  ventricular  contraction  (Fig.  49),  except 
where  the  rate  i?  fast,  for  then  it  is  apt  to  vanish.     Aortic 
murmurs  obey  the  general  rule,  their  presence  or  absence  is 
controlled  by  the  efficiency  of  the  respective  beats  (Fig.  47). 
The  inactivity  of  the  auricle  is  responsible  for  special 
alterations  of  the  heart  sounds  in  patients  who  have  stenosis 
of  the  mitral  orifice.     It  is  customarj?^  to  allude  to  disappear- 
ance of  presystolic  murmurs  when  the  auricle  fibrillates,  but 
this  statement  is  not  exact.     The  change  in  the  characters  of 
the  murmurs  at  the  onset  of  fibrillation  is  oftentimes  impres- 
sive, but  it  varies  according  to  the  heart  rate  and  the  degree 
of  stenosis.     If  there  are  short  presystolic  murmurs  while 
the    heart    beats    regularly,  these    murmurs  usually  vanish 
when   fibrillation   begins  ;  and   more   especially   if   the   rate 
during    fibrillation    is    rapid.     If    the    presystolic    murmur 
is  long  and  rough,  a  murmur  of  similar  character  is  preserved 
during    fibrillation.       But    its    time    relations    are    altered. 
Attention    should    concentrate    upon    the    position    of    the 
second  sound  at  the  apex.     When  the  auricle  is  fibrillating, 
the  diastolic  murmur  has  a  fixed  time  relation  to  this  sound. 
If  the  heart  is  rapid,  the  murmur  begins  early  in  diastole 
and  fills  the  whole  gap  to  the  first  sound  of  the  succeeding 
beat  (Fig.  48)  ;  if  the  heart  rate  is  less  rapid,  the  murmur 
maintains  its  relation  to  the  second  sound  but  falls  short  of  the 
succeeding  first  sound  during  the  longest  ventricular  pauses 
(Fig.  4:Qp)  ;  if  the  heart  rate  is  slow,  a  long,  though  varying, 
interval  separates  the  end  of  the  murmur  and  the  next  first 
sound  ;    the    murmur    is    then    confined    to    early    diastole 
(Fig.  50),  and  often  acquires  a  soft  quality,  making  it  difficult 


Auricular  Fibrillation.  99 

to  distinguish  it  from  that  of  aortic  regurgitation.  The 
whole  series  of  murmur  arrangements  may  be  observed 
in  a  single  case  which  exhibits  different  heart  rates  from 
time  to  time.  The  reason  of  the  changes  will  be  clear  when 
the  pressures  and  mechanism  are  considered.  The  diastoUc 
murmurs  of  mitral  stenosis  are  dependent  upon  the  rate 
of  flow  through  the  constricted  orifice,  and  the  rate  of  flow 
is  controlled  by  the  difference  of  pressure  in  auricle  and 
ventricle  at  any  given  moment.  Now,  although  the  auricular 
pressure  exceeds  the  ventricular  during  the  whole  of  diastole, 
the  excess  is  greatest  at  two  phases,  namely,  when  the 
auricle  is  in  contraction  and  directly  after  the  opening  of  the 
auriculo -ventricular  valves.  When  the  auricle  contracts  in 
normal  fashion,  mitral  diastoUc  murmurs  are  in  chief  evidence 
at  first  in  late  and  afterwards  in  early  diastole  ;  they  are 
found  in  early  diastole  when  the  auricle  is  virtually  paralysed, 
especially  when,  the  heart  rate  being  slow,  stasis  raises  the 
ventricular  pressure  during  the  last  phases  of  diastole. 

Auricular  fibrillation  msij  be  recognised  clinically  by  the 
nature  of  the  ventricular  action,  but  its  detection  is  aided, 
as  we  have  seen,  by  other  signs.  It  is  possible  to  formulate 
a  few  general  rules  which  serve  as-  most  useful  guides  in 
identifying  it.  When  the  ventricle  beats  irregularly  at  a 
rate  surpassing  120  per  minute,  the  irregularity  is  almost 
always  of  this  nature.  When  an  irregular  ventricular  action 
accompanies  signs  and  symptoms  of  serious  heart  failure  it 
is  probably  the  result  of  auricular  delirium,  and  the  proba- 
bility is  increased  if  the  heart  rate  is  much  accelerated.  In 
patients  in  whom  the  heart  is  irregular,  but  in  whom  the 
heart  rate  is  not  much  accelerated,  and  in  whom  signs  of  heart 
failure  are  absent  or  few,  a  test  may  be  applied  which  is  of 

h2 


100  Chapter    V  1 1. 

considerable  value.  Moderate  exercise  or  the  administration 
of  amyl  nitrite  augment  the  ventricular  rate,  and  this  is 
so  whether  fibrillation  is  present  or  not  ;  but  there  is  a 
striking  contrast  in  two  given  cases  of  irregularity,  of  which 
one  is  due  to  auricular  fibrillation,  while  the  other  has  a 
different  cause  {i.e.,  extrasy stoles,  partial  heart-block,  etc.). 
In  fibrillation  the  pulse  becomes  more  irregular  with  its 
acceleration,  while  in  the  remainder  the  pulse  steadies  in 
rhythm.  When  premature  beats  are  present,  a  sufficient 
acceleration  of  ventricular  rate  to  abolish  them  temporarily 
maj^  often  be  induced  by  several  quick  changes  from  the 
recumbent  to  the  sitting  posture  ;  this  is  not  so  where 
fibrillation  is  concerned.  Conversely,  as  the  pulse  shows 
subsequent  to  exercise,  the  irregularity  of  fibrillation  decreases, 
while  other  forms  of  irregularity  become  more  prominent. 
Fever  similarly  raises  the  ventricular  rate,  and  during  the 
febrile  stage  the  disorder  of  fibrillation  persists  and  is  often 
augmented  in  degree.  A  study  of  the  relation  of  irregularity 
to  heart  rate  is  the  quickest  and  the  most  certain  means  by 
which  auricular  fibrillation  can  be  recognised  cHnically. 
It  does  not  matter  how  the  rate  is  raised,  providing  it  goes 
beyond  120  per  minute,  and  the  irregularity  remains,  the 
diagnosis  is  almost  certain  ;  and  as  the  rate  is  higher  so  the 
diagnosis  becomes  more  certain.  Another  cHnical  test 
which  I  have  often  employed  with  success  is  based  on  the 
absence  of  a  respiratory  control  of  rate.  However  deeply 
the  patient  breathes,  quickening  of  the  pulse  fails  to  fall 
regularly  in  the  respiratory  phases,  as  it  does  in  all  other 
forms  of  heart  irregularity,  with  the  exception  of  those 
due  to  auricular  flutter.  Finally,  the  persistence  of  the 
irregularity,  which  is  due  to  fibrillation,  needs  emphasis.     In 


Auricular  Fibrillation.  101 

most  cases  it  is  continuous  from  the  time  of  observation  until 
death.  The  other  irregularities  are  present  from  time  to 
time,  so  that  there  are  intervals  of  regular  ventricular  action 
each  hour  or  each  day. 

Auricular  fibrillation  is  recognisable  by  means  of  these 
tests  and  without  the  aid  of  graphic  methods  in  over  90  per 
cent,  of  the  patients  in  whom  it  occurs. 

The  general  symptomatology. 

The  symptoms  complained  of  by  patients  in  whom  the 
auricles  fibrillate  are  various,  being  dependent  mainly  upon 
the  concomitant  conditions.  For  the  most  part,  they  are 
the  symptoms  of  degenerate  and  failing  heart  muscle,  and 
these  do  not  require  reiteration  at  the  present  time.  The 
symptoms  which  are  now  our  special  concern  are  those 
which  appear  to  be  the  special  effects  of  fibrillation  itself. 
Patients  who  possess  the  persistent  disorder  often  experience 
occasional  fluttering  in  the  chest  and  neck  and  may  be 
conscious  of  irregular  heart  action.  They  are  more  prone 
to  shortness  of  breath,  exhaustion  and  other  symptoms 
of  over-taxation  of  the  heart  than  are  those  with  similar 
valve  lesions  and  a  like  degree  of  cardiac  dilatation*  ;  but  it 
is  not  always  easy  to  allot  these  superadded  symptoms  to 
precise  causes  ;  they  are  in  part  the  result  of  the  graver 
myocardial  condition  which  consorts  with  fibrillation  ;  they 
•are  in  part  due  to  the  actual  turbulence  and  embarrassment 
of  the  ventricular  movements."]'  We  know  that  the  heart  is 
taxed  by  its  disorderly  action,  but  it  cannot  be  stated  that  any 

*  On  the  other  hand,  they  seem  peculiarly  exempt  from  angina. 

t  The  heart  embarrassment  is  the  result  of  ventricular  irregularity  and 
especially  of  rapid  action  ;  the  virtual  paralj'sis  of  the  auricle  is  probably 
without  appreciable  effect  on  the  general  circulation. 


102  Chapter    VII. 

symptom,  such  as  cyanosis,  conspicuous  dyspnoea,  noticeable 
venous  engorgement  or  dropsy,  is  the  direct  outcome  of 
fibrillation  alone  ;  for  cardiac  failure  and  these,  its  classical 
accompaniments  are  to  be  found  where  there  is  no  fibrillation, 
and  instances  of  fibrillation  are  common  in  which  these 
symptoms  have  not  developed.  The  symptoms,  as  has  been 
stated,  are  provoked  bj^  the  interplay  of  two  factors,  namely, 
the  inherent  muscle  defect  and  the  extra  burden  of  disordered 
and  rapid  action  ;  while  the  signs  of  failure  are  jiroportioned 
to  the  degree  of  muscle  damage,  the  wh©le  of  this  symptomatic 
scale  is  raised  by  rapid  heart  action.  In  the  healthy  hearts  of 
animals  it  is  a  general  rule  that  fibrillation  of  the  auricle 
produces  a  fall  of  arterial  and  a  sHght  rise  of  venous  pressure, 
but  at  the  same  time  it  is  accompanied  by  a  decrease  in  the 
heart's  dimensions,  a  usual  phenomenon  when  the  rate  is 
increased.  The  heart  accommodates  itself  to  the  new 
conditions  in  a  few  moments  ;  the  arterial  pressure  rises  and 
the  venous  pressure  falls,  so  that  they  almost  recover  their 
previous  levels  and  the  blood  flow  is  maintained  in  a  well-nigh 
perfect  fashion.  But  if  the  heart  has  been  damaged,  the 
effect  is  both  profound  and  lasting,  and  in  place  of  decrease 
of  heart  volume,  an  increase  may  occur.  So  it  is  in  patients. 
Patients  may  experience  paroxysmal  fibrillation  at  intervals 
of  a  month  or  perhaps  a  year  ;  many  of  them  pass  through 
their  attacks  with  little  or  no  sensibility  of  them  ;  neither 
can  any  sign,  other  than  the  disordered  action,  be  discovered 
during  their  progress.  Yet  similar  crises  give  rise  in  other 
patients  to  profound  and  serious  disturbance,  breathlessness, 
pain,  cyanosis,  and  further  indications  of  increasing  dilatation 
of  the  heart. %  In  these,  the  severest  cases,  the  symptoms 
resemble    those    of    long    continued    paroxysms    of    regular 


Auricular   Fibrillation,  103 

tachycardia.  Between  the  mild  and  most  extreme  reactions  is 
the  intermediate.  The  variation  in  the  reaction  is  great,  and, 
as  I  have  said,  is  largely  attributable  to  the  grade  of  underlying 
muscle  weakness.  But  there  is  another  and  equally  important 
factor  in  the  human  subject ;  it  is  the  grade  of  the  ventricular 
disorder  during  the  attack.  Just  as  the  muscle  defect  varies 
in  its  degree,  so  also  does  the  burden  imposed  upon  it ; 
thus  it  is  found  that  Uttle  reaction  is  shown  in  paroxysms 
of  relatively  slow  ventricular  action,  while  amongst  those 
with  grave  disturbance  the  ventricular  rate  is  usually  rapid. 
Influence  upon  thrombosis  and  infarction.  If  a  series 
of  diseased  hearts  is  examined  at  autopsy,  ante-mortem  clots 
are  found  in  much  the  heavier  percentage  in  those  auricles 
which  during  Hfe  exhibited  fibrillation.  The  virtual  paralysis 
of  the  auricles,  and  the  consequent  stagnation  of  blood  in  them, 
definitely  predisposes  to  thrombosis  in  the  appendices.  Yet 
in  mitral  stenosis  hsemoptysis,  the  result  of  lung  infarction, 
appears  to  be  no  commoner  where  fibrillation  exists  than 
where  the  natural  ryhthm  is  preserved.  The  explanation 
seems  to  be  that  although  fibrillation  aids  the  formation  of 
clots,  the  passivity  of  the  auricular  walls  safeguards 
these  clots  from  detaching.  In  paroxysmal  fibrillation  I  have 
observed  a  coincidence  between  emboKsm  of  lungs  and  brain 
and  the  resumption  of  the  normal  auricular  contractions. 
Presumably,  clots  formed  during  the  period  of  auricular 
fibrillation  are  detached  if  and  when  the  heart  resumes  its 
natural  mode  of  beating. 

Remarks  upon  diagnosis. 
The  diagnosis,  often  suggested  for  cases  which  exhibit 
fibrillation  of  the  auricles,  is  still  that  of  the  accompanying 


104  Chapter    VII. 

valve  lesion,  though  I  am  strongly  of  opinion  that  it  is  no 
longer  warrantable.  A  diagnosis  should  include  either  the 
outstanding  feature  of  the  pathology,  or  it  should  be  chosen 
that  it  may  become  associated  with  some  specially  beneficial 
form  of  treatment.  In  these  patients  a  chronic  affection 
of  the  myocardium  is  the  essential  lesion  ;  while  the  relations 
of  the  cardiac  disorder  to  digitalis  medication  are  so  peculiar 
that  the  named  disorder  of  the  heart  always  brings  this 
drug  to  mind. 

But  I  wish  to  refer  but  briefly  to  this  question  of 
terminology  under  the  present  heading,  having  chosen  it 
to  emphasise  a  common  and  avoidable  diagnostic  blunder  ; 
this  comes  from  want  of  true  apj)reciation  of  the 
mechanism  in  these  cases.  In  discussing  the  signs  associated 
Avith  fibrillation,  I  have  spoken  of  the  modification  of 
diastoHc  murmurs  in  mitral  disease.  A  murmur,  which 
originally  occupies  the  full  diastole  of  the  shorter  cycles,  is 
replaced  as  the  heart  slows  by  an  early  diastolic  murmur 
which  is  maximal  in  the  region  of  the  apex.  It  is  the  last 
murmur  which  so  frequently  misleads  the  physician  and 
suggests  to  him  an  insufficiency  of  the  aortic  valves.  It  is 
said  that  in  some  cases  of  aortic  regurgitation  the  character- 
istic bruit  is  confined  to  the  apex,  but  this  is  certainly  far  less 
common  than  has  been  supposed,*  and  an  erroneous  concep- 
tion of  its  frequence  has  arisen  from  inclusion  of  many  of 
the  cases  to  which  I  now  refer.  When  mitral  stenosis  and 
auricular  fibrillation  are  present  in  the  same  patient,  and  the 
heart  rate  is  slow,  an  early  diastolic  murmur,  most  clearly 
audible  at  the  apex  but  often  audible  around  and  above  it,  is 


*  Without  actually  denying  its  occurrence,  I  can  but  state  that  I  have 
yet  to  see  an  example  of  it. 


Auricular   Fibrillation.  105 

an  expected  sign.  A  diagnosis  of  aortic  reflex  is  never  justifi- 
able when  the  lieart  is  grossly  irregular  and  slow,  unless 
unequivocal  signs  of  it  are  present  apart  from  such  a  murmur. 
UncompHcated  aortic  valvular  disease  and  fibrillation  of  the 
auricles  is  a  comparatively  rare  clinical  picture.  The 
combination,  yielding  a  purel}^  apical  murmur,  is  so  far  an 
undescribed  condition.  Close  attention  to  the  character  and 
accurate  timing  of  the  adventitious  sound  is  often  helpful. 
The  early  diastohc  murmur  of  mitral  stenosis  is  relatively  low 
in  pitch  and  it  usually  begins  a  little  later  than  the  second 
sound.  The  absence  of  a  waterhammer  pulse  and  of  a 
murmur  at  the  aortic  cartilage  should  indicate  the  mitral 
valve  as  the  probable  seat  of  mischief. 

The  p7-ognosis. 

As  in  all  other  kinds  of  heart  irregularity,  the  prognosis 
is  largely  governed  by  the  remaining  symptoms  and  signs, 
and  in  any  individual  case  an  estimate  is  formed,  which 
includes  consideration  of  the  past  history,  the  presence  or 
absence  of  serious  symptoms  and  their  relation  to  exercise, 
the  presence  or  absence  of  enlargement,  of  valve  lesion,  renal 
disease,  etc..  Fibrillation  is  in  many  cases  significant  in  that 
it  is  the  chief  or  only  rehable  sign  that  the  heart  muscle  has 
been  affected.  It  is,  as  I  have  said,  in  itself  an  evidence  of 
muscular  damage.  In  most  cases  it  heralds  cardiac  failure, 
temporary  or  terminal,  so  that  few  patients  survive  its  onset 
for  more  than  ten  years.  There  are  well  authenticated 
instances  in  which  it  has  persisted  for  a  longer  period,  but 
they  are  few.  A  persistent  ventricular  rate  of  120  or  over 
is  of  serious  omen,  and  according  as  the  rate  is  maintained 
above  this  count,  so  the  outlook  becomes  graver,  providing 


106  Cha'pter    VIL 

that  the  patient  remains  untreated.  Rates  of  140  and  over 
are  rarely  maintained  for  many  months,  rates  of  160  do  not 
continue  for  many  weeks.  Such  extra  loads  are  not  tolerated 
by  a  defective  muscle.  An  extremely  important  consideration 
is  therefore  the  reaction  to  treatment.  As  we  shall  see,. 
most  of  these  cases  react  to  cardiac  drugs  ;  in  many — prob- 
ably in  all  where  the  original  rate  is  much  in  excess  of" 
normal — the  rate  can  be  controlled,  being  reduced  and 
maintained  within  Umits  which  spare  the  heart  excessive 
taxation  of  its  strength.  In  deahng  with  a  patient  who  has 
a  given  heart  rate,  the  prognosis,  in  so  far  as  it  is  affected: 
by  the  fibrillation,  does  not  depend  so  much  upon  the  heart 
rate  first  observed  as  upon  the  heart  rate  which  persists  under 
treatment. 

If  two  patients  showing  equal  signs  of  cardiac  failure 
differ  in  that  the  one  presents  a  normal  rhythm,  while  the  other 
manifests  a  rapid  ventricular  action,  the  result  of  fibrillation, 
then  the  prognosis  is  more  favourable  in  the  latter ;  for  in  him 
the  heart  is  burdened  by  a  load  which  treatment  will  remove^ 

The  treatment. 

There  is  no  other  serious  cardiac  disorder  which  may  be 
so  speedily  benefited  as  the  Avell-managed  case  of  auricular 
fibrillation.  In  no  other  cardiac  affection  can  the  medical 
attendant  point  with,  more  thorough  confidence  to  the  effects 
of  his  remedies.  As  a  direct  result  of  active  treatment  the 
moribund  may  be  restored,  and  many  years  may  be  added  to 
their  lives.  Auricular  fibrillation  is  the  condition  to  wliich 
drugs  of  the  digitalis  group  almost  exclusivel}^  owe  their 
well-founded  reputation. 


Auricular  Fibrillation.  107 

The  guide  to  the  physician  is  the  rate  of  the  heart  beat, 
an  index  which  rarely  fails  him.  Auricular  fibrillation  is  an 
absolute  indication  for  the  administration  of  a  member  of  the 
digitalis  group,  whenever  the  heart  rate  exceeds  100  while 
the  patient  is  at  rest.  In  most  of  these  patients  the  drug 
acts  as  a  specific,  impeding  the  passage  of  impulses  from 
auricle  to  ventricle  and  thus  reducing  the  ventricular  rate. 
If  the  heart  rate  does  not  fall  as  a  result  of  rest,  and  if  it  does 
not  fall  when  digitahs  or  an  alhed  drug  has  been  properly 
administered,  no  other  remedy  is  known  which  is  of  service 
in  reducing  the  heart  rate.  In  young  people,  and  especially 
those  who  have  been  affected  by  rheumatism  or  chorea,  it  is 
certain  that  an  absolute  control  of  the  rate  can  almost  always 
be  estabUshed  and  maintained.  The  treatment  consequently 
consists  of  the  administration  of  such  doses  as  will  keep  the 
heart  rate  within  reasonable  limits.  As  more  experience  is 
gained  of  this  treatment,  the  fewer  become  the  failures  ; 
cases  in  which  the  heart  rate  fails  to  respond  to  full  doses 
are  now  known  to  be  very  rare. 

It  does  not  necessarily  follow  that  a  patient  who  has 
fibrillation  should  lie  up.  But  where  the  average  heart  rate 
exceeds  100  it  is  advisable,  and  the  patient  should  remain  in  bed 
until  his  reaction  to  digitalis,  or  a  similar  drug,  has  been 
thoroughly  investigated.  Further  treatment  in  bed  is  decided 
upon  according  to  the  general  condition,  and  according  to  the 
tolerance  and  reaction  to  digitahs.  In  all  where  a  high 
ventricular  rate  obtains,  a  reaction  is  speedily  forced.  These 
latter  may  be  divided  into  three  classes  :  the  first,  those  in 
whom  the  reaction  is  a  permanent  one  ;  these  are  patients  in 
whom  the  rate  remains  sIony  though  digitalis  is  omitted  ;  they 
are    comparatively   rare  :  the    second,    those   in   whom    the 


108  Chapter    VII. 

reaction  is  permanent  when  small  closes  are  subsequently 
administered  :  the  third,  those  in  whom  relatively  high  dosage 
is  persistently  required  to  maintain  control. 

As  a  routine,  the  tincture  or  fresh  infusion  of  digitalis 
is  given,  for  it  is  a  safe  and  most  potent  remedy.  The 
tincture  is  given  to  adults  in  doses  of  from  10  to  20  minims 
three  or  four  times  a  day  (the  infusion  in  1  to  1^-  drachm 
doses)  ;  if  the  reaction  does  not  begin  within  four  or  five  days, 
the  dosage  should  be  maintained  or  even  increased  until 
symptoms  of  nausea,  diarrhoea,  headache  or  pulse  slowing 
appears.  It  usually  happens  that  the  desired  fall  of  heart  rate 
first  comes  just  before  or  at  the  time  when  other  signs  of 
intoxication  are  manifested  ;  if  these  persist  for  several  days 
the  drug  must  be  reduced  or  omitted,  whether  the  rate  has 
fallen  or  not.  The  dosage  is  also  to  be  reduced  if  the  heart 
rate  falls,  and  the  reduction  is  continued  so  long  as  the  heart 
rate  remains  below  80.  The  quantity  may  be  diminished  to 
nothing  in  many  cases  ;  often  5  or  7  minim  doses  eventually 
suffice.  Usually  the  full  reaction  is  obtained  after  six  or 
eight  drachms  of  the  tincture,  or  an  equivalent  quantity  of 
infusion,  has  been  given.  Whenever  the  average  rate  has 
reached  00  to  80  per  minute,  the  drug  is  stopped,  and  it  is 
given  again  only  if  the  heart  rate  begins  to  accelerate  once 
more.  The  appearance  of  coupled  heart  beats  (Fig.  50)  is 
always  a  sign  of  danger  ;  whenever  they  appear*  the  digitahs 
must  be  discarded.  I  have  seen  more  than  one  case  of  un- 
expected death,  attributable  to  continued  dosing  with  digitalis 
after  this  stage  has  been  reached ;  it  must  be  remembered 
always  that  digitalis  is  a  poison,  and  that  it  has  other 
actions  than  the  simple  reduction  of  heart  rate. 

*  They  do  not  usually  appear  until  the  rate  has  been  reduced  below  the 
justifiable  limits. 


Auricular  Fibrillation.  109 

In  the  average,  it  may  be  said  that  a  patient  will  usually 
use  up  or  excrete  some  15-20  minims  of  the  tincture  daily, 
and  that  it  is  not  until  such  doses  are  exceeded  that  accumu- 
lation of  the  drug  occurs  in  the  body.  To  produce  the  full 
effects,  and  that  is  often  necessary,  an  average  quantity  of 
5  drachms  has  to  be  accumulated.  This  is  accomplished  by 
giving  7  drachms  over  a  period  of  7  days.  With  5  to  7  minim 
doses  there  is  usually  no  accumulation,  but  a  previous 
accumulation  may  be  maintained  by  these  amounts. 

In  some  instances  where  the  patient  has  reacted,  the 
drug  can  be  stopped  without  the  rate  re-accelerating  so  long  as 
he  remains  in  bed.  When  he  rises  from  bed  a  renewal  of  the 
small  dose  (5  to  7  minims)  may  be,  and  usually  is,  necessary. 
In  other  cases  the  result  is  less  satisfactory  and  heavier  dosage 
must  continue.  The  administration  of  digitahs  in  small  or 
moderate  doses  may  be  continued  beneficially  for  years  in 
many  patients. 

It  sometimes  happens  that  a  patient  is  pecuHarly 
intolerant  to  digitahs,  and  that,  where  a  reaction  is  expected, 
a  dosage  of  15  to  20  minims  of  the  tincture  cannot  be  reached 
or  maintained  sufficiently  long,  without  nausea  or  other 
discomforting  symptoms  supervening.  The  drug  should  be 
diluted  and  given  directly  after  meals.  Strophanthus  (in  its 
new  B.P.  strength)  or  squills  may  be  tried,  starting  with 
doses  of  10  minims  or  20  minims  of  the  respective  tinctures. 
These  drugs  are  pushed  in  the  same  manner,  but  though 
they  are  less  apt  to  induce  nausea  or  vomiting,  and  while 
diarrhoea  is  the  chief  disturbance  produced  by  them,  they 
are  less  reliable  than  digitalis.  In  some  of  these  cases, 
too,  recourse  may  be  had  to  intravenous  injections  of 
strophanthin. 


110  Chapter    VII. 

When  a  patient  who  has  fibrillation  is  first  seen,  and  the 
heartbeats  persistently  at  170-200  per  minute,  the  condition 
is  urgent  and  heavy  doses  of  digitalis  (20  to  30  minims)  should 
be  employed.  The  intravenous  injection  of  strophanthin 
is  also  valuable  at  such  times.  Two,  or  not  more  than  three, 
doses  of  1/250  of  a  grain,  each  in  40-60  minims  of  saHne,  are 
given  at  intervals  of  two  hours.  The  reduction  of  rate 
begins  almost  at  once,  and  heart  rates  of  90  or  80  are  reached 
in  from  6-12  hours.  The  remedy  should  be  employed 
cautiously,  and  its  adoption  must  be  confined  to  the  urgent 
case  Avith  very  high  ventricular  rates,  or  to  cases  in  which 
medication  by  the  mouth  has  been  hindered  by  the  onset  of 
gastro-intestinal  symptoms. 

The  treatment  of  the  case  of  auricular  fibrillation  in  the 
patient  who  is  up  and  about  is  guided  mainly  by  the  rate  of 
the  heart  and  the  urgencj^^  of  the  patient's  symptoms.  The 
disorder  is  generally  persistent,  and  most  hospital  patients 
eventually  leave  their  beds  and  return  to  their  former  or 
somewhat  fighter  occupations  ;  the  latter  are  naturally 
advised.  But  even  where  the  pulse  rate  is  persistently 
low  and  symptoms  are  few,  excessive  exertion  should  be 
avoided  ;  heavy  manual  labour,  strenuous  games  and  sports 
should  form  no  further  part  in  the  daily  fife.  If  the  pulse  rate 
quickens  readily,  if  drugs  are  constantly  required  to  maintain 
a  low  ventricular  rate,  and  especially  if  breathlessness  or 
precordial  uneasiness  are  easily  induced,  further  restrictions 
are  necessary.  All  patients  of  the  female  sex  should  be 
specially  warned  of  the  strain  and  danger  of  pregnancy. 

Regular  meals,  consisting  only  of  a  sufficiency  of  solid 
and  sustaining  food,  preferably  dry,  early  hours,  a  placid 
existence,  the  avoidance  of  public  buildings  and  all  places 


Auricular  Fibrillation.  Ill 

-and  seasons  in  which  influenza  and  bronchitic  troubles  are 
contracted,  and,  lastly,  scrupulous  attention  to  the  hygiene 
of  the  teeth  and  throat,  are  sound  directions  in  this  as  in 
•other  serious  heart  maladies. 

Belladonna,  its  ally  hyoscyamus  and  their  extractives 
.should  be  avoided.  Their  customary  action  is  to  increase  the 
rate  of  the  ventricle  in  this  condition. 

In  cases  of  urgency,  or  where  the  patient's  life  may  be 
■considerably  prolonged  by  surgical  operation,  general  anses- 
"thetics  may  be  employed.  But  where  there  is  any  hesitancy 
to  perform  an  operation,  apart  from  the  cardiac  condition, 
the  presence  of  fibrillation  should  countermand  it. 

Paroxysmal  fibrillation. 

Most  auricles  which  develop  fibrillation  maintain  this 
mechanism  to  the  end  of  the  chapter ;  it  is  essentially 
a  chronic  and  at  last  a  terminal  malady.  But  from  time  to 
i:ime  transient  attacks  are  seen,  and  in  some  patients 
paroxysms  of  fibrillation  lasting  a  few  hours,  days  or  weeks 
-are  noted.  The  affection,  when  it  takes  this  form,  is  generally 
■classed  as  paroxysmal  tachycardia.  In  my  discussion  of 
paroxysmal  tachycardia  I  have  excluded  it,  desiring  to  deal, 
-as  I  did,  with  the  simpler  mechanism  alone. 

The  frequence  of  the  paroxysmal  affection  may  be 
gauged  approximately  by  comparison.  Of  the  152  cases  of 
-auricular  fibrillation  included  in  the  table  on  page  93,  in  only 
16  was  the  disorder  temporary  and  recurring.  Paroxysms  of 
regular  tachycardia  appear  to  be  more  common  ;  while  the 
16  irregular  tachycardias  were  being  collected,  simple  and 
regular  paroxysms  were  seen  in  45  patients. 


1,12  Chapter    VII. 

The  symptoms  of  paroxysmal  fibrillation  have  been 
spoken  of  already.  They  may  be  inconspicuous  or  profound. 
When  the  rate  of  ventricular  response  is  rapid  (160-200  per 
minute)  the  symptoms  are  those  of  simple  tachycardias 
at  similar  rates,  though  the}^  are  on  the  \Ahole  more  severe. 
The  prognosis  is  reasoned  in  the  manner  stated  for  regular 
paroxysms  ;  the  management  and  symptomatic  treatment  of 
the  attacks  are  similar  in  the  two.  A  few  words  are  necessary 
upon  chgitahs  medication.  Drugs  belonging  to  this  group 
have  been  known,  not  infrequently,  to  excite  fibrillation  in 
those  predisposed.  In  general  they  are  therefore  contra- 
indicated  in  paroxysms  of  short  duration.  When  the 
paroxysm  of  fibrillation  is  prolonged  and  lasts  for  fourteen 
days,  the  fibrillation  may  be  regarded  as  permanent  and 
treated  as  is  the  persistent  condition.  In  urgent  paroxysms, 
where  high  ventricular  rates  prevail,  digitahs  medication 
may  be  adopted  with  advantage  ;  the  dosage  should  be 
arranged  for  a  speedy  reaction.  The  drug  affords  quick 
relief,  though  bj''  its  use  the  duration  of  the  attack  ma}''  be 
prolonged. 

A c  lite  fibrillation . 

Fibrillation  of  the  auricles  sometimes  intervenes  during 
the  course  of  acute  infections  and  continues  for  a  few 
moments,  hours  or  days.  I  have  witnessed  attacks  of  this 
kind  in  severe  tonsilitis,  acute  cholecystitis,  acute  appendi- 
citis, infective  endocarditis  and  pericarditis,  and  others  have 
been  reported  in  scarlet  fever  and  in  pneumonia. 


(      113     ) 


Chapter  VIII. 

ALTERNATION   OF   THE   HEART. 

Definition. 

A  condition  in  which  the  left  ventricle,  while  beating 
with  regular  rhythm,  expels  larger  and  smaller  quantities  of 
blood  at  alternate  contractions. 

The  inechanism  in  alternation  of  the  heart. 
Alternation    in    the   size   of  pulse   beats,   so  that  each 
alternate  beat  is  large  and  each  alternate  beat  is  small,  is  of 
obscure  origin.    The  contractions  of  the  ventricle  are  regular. 


A 


Fig.  51.  A  diagrammatic  representation  of  alternation  of  the  heart.  The 
aiiricular  and  ventricular  beats  are  placed  regularly  and  in  order,  but 
alternate  ventricular  contractions  are  weak. 


and  each  is  preceded  at  a  normal  interval  by  a  contraction  of 
the  auricle  (Fig.  51).  The  disturbance  is  dependent  upon 
an  anomaly  of  the  ventricular  systoles,  whereby  at  each 
alternate  systole  of  the  left  ventricle  a  greater  or  lesser 
quantity  of  blood  is  thrown  into  the  systemic  arteries.     In 


114  Glmpter    VIII. 

the  ligure,  I  have  represented  this  anoinal}''  b\'  varying  the 

size  of  the  ventricular  rectangles.     The  hypothesis  is  that  a 

different  number  of  the  ventricular  fibres  contract  at  alternate 

systoles. 

Etiological  and  pathological  relations. 

Alternation  of  the  pulse  is  seen  in  two  classes  of  patient. 
First,  it  occurs  in  those  in  whom  the  lieart  rate  is 
unduly  accelerated  and  more  especially  as  an  accompaniment 
of  paroxysmal  tachycardia.  Associated  with  paroxysmal 
tachycardia,  it  has  etiological  and  pathological  relations  in 
common  mth  the  last  named  disorder  ;  its  prognostic  signifi- 
cance is  in  these  circumstances  neghgible.  depending  as  it  does 
chiefly,  if  not  entirely,  upon  acceleration  of  the  lieart  rate. 
It  may  be  regarded  almost  as  a  physiological  reaction  to  the 
increased  frequency  of  the  heart  beat. 

Secondly,  it  occurs  when  the  heart  rate  lies  within 
normal  hniits  and  at  such  times  it  is  a  sign  of  considerable 
import.  Seen  in  elderly  subjects  and  pre-eminently  in  the 
male  sex,  it  consorts  especially  with  angina  pectoris,  high 
arterial  pressure,  renal  disease,  and  a  fibrotic  myocardium. 
It  has  been  seen  in  pneumonia  during  the  pre-critical  stage, 
and  also  in  patients  under  the  influence  of  large  doses  of 
digitahs. 

Alternation  of  the  heart  is  encountered  in  experiment 
under  similar  circumstances,  namely,  when  the  heart  rate  is 
extremely  rapid,  or  when  the  organ  has  been  injured  bj^  the 
intravascular  injection  of  poisons.  Whenever  it  occurs, 
there  is  reason  to  believe  either  that  a  tolerably  healthy  heart 
muscle  is  carrying  an  excessive  burden,  or  that  a  diseased  or 
poisoned  muscle  is  struggling  to  perform  work  of  which  it  is 
barely  capable. 


Alternation  of  the   Heart.  ]  1 5 

In  the  remainder  of  this  chapter  I  shall  allude  to  pulse 
alternation  as  an  accompaniment  of  heart  rates  which  are 
not  high.  When  the  heart  is  disposed  to  alternate,  the 
actual  alternation  is  unmasked  by  anything  which  imposes  a 
fresh  and  added  strain  upon  that  organ.  Thus  it  is  often 
made  manifest  by  a  slight  acceleration  of  pulse  rate  ;  and 
in  the  earlier  stages  of  its  development,  it  is  frequently 
exposed  by  single  premature  beat  ;  in  the  last  named 
circumstance  it  follows  immediately  upon  the  extrasystole, 
and  continues  for  a  varying  number  of  heart  cycles. 


Fig.  52.     Alternation  of  the  pulse.     Each  alternate  beat  is  strong  and  each 
alternate  beat  is  weak. 


t  ^   I  ^  ■    ^^^'"^ 

Fig.  53.  Apex  and  radial  curves  and  heart  sounds  in  heart  alternation. 
The  curve  is  taken  at  a  faster  rate  than  the  last  and'  shows  the  slight 
variation  in  pulse  pauses.  As  opposed  to  the  picture  when  premature 
beats  are  puesent,  the  stronger  beat  is  followed  bj^  the  longer  pause. 

It  is  an  affection  of  advancing  years,  its  heaviest  inci- 
dence being  in  the  fifth,  sixth  and  seventh  decades  ;  it  is  much 
commoner  in  men  than  in  women.  Dr.  White,  of  Boston, 
who  collected  seventy-one  cases  in  eight  months,  considers 
it  is  as  frequent  as  fibrillation  of  the  auricles  ;  certainly  it 
is  a  common  disorder,  generally  passing  unobserved. 


116  Chapter    VIII. 

The  recognition  of  pulsus  alternans. 

It  is  unfortunate,  but  true,  that  most  instances  of 
pulsus  alternans  cannot  be  recognised  other  than  by 
instrumental  means.  There  are  patients  in  whom  it  affects 
the  pulse  continuously,  and  in  whom  alteration  in  the  force 
of  alternate  pulse  beats  is  perceptible  to  the  finger*  ;  but 
such  cases  are  rare,  and  the  feel  of  the  pulse  should  not 
be  trusted.  Examination  of  the  cardiac  impulse  gives  little 
assistance,  for  the  heart  beats  with  regular  rhythm  and  the 
differences  in  the  force  of  ventricular  systoles  and  the  intensity 
of  the  heart  sounds  are  inappreciable. 

The  systolic  pressure  of  the  large  beats  is  several  milli- 
metres higher  than  that  of  the  small  beats ;  by  nicely 
regulating  the  pressure  in  the  armlet  of  the  sphygmomano- 
meter, the  smaU  beats  may  be  hindered  from  passing,  and  the 
pulse  rate  below  the  armlet  is  thus  halved. 

It  is  a  sign  of  such  importance  and  is  so  readily 
overlooked,  that  it  should  be  sought  deliberately  when 
there  is  reason  to  suspect  its  presence.  Thus  it  is  wise  to 
examine  all  cases  of  angina  pectoris,  all  cases  of  high  blood 
pressure  and  all  elderly  subjects  in  whom  affection  of  the 
heart  is  suspected,  or  renal  disease  is  known  to  exist,  with 
a  specific  object,  namely,  to  determine  its  presence  or  absence. 
It  should  be  looked  for,  too,  in  all  elderly  people  in  whom 
premature  beats  are  frequent.  If  such  methods  are  adopted 
it  wiU  not  often  escape  detection.  It  is  so  frequently  con- 
fined to  the  few  cycles  which  follow  a  premature  beat  that; 
in  any  class  of  the  patients  mentioned,  it  is  important  to 
obtain  a  curve  wliich  contains  such  a  beat.     This  may  often 

*  The  separation  from  a  dicrotic  pxilse  is  easy  ;  for  where  the  latter  is- 
present  the  beating  of  the  pulse  is  at  twice  the  rate  of  the  ventricle. 


Alternation  of  the   Heart.  117 

happen  at  the  first  examination.  The  patient  should  remain 
standing,  for  premature  beats  are  more  frequent  in  this  pos- 
ture, and  if  he  has  come  some  distance  it  is  well  that  the 
examination  should  proceed  at  once,  since  premature  beats 
are  more  conspicuous  at  such  times.  It  should  be  remem- 
bered, too,  that  a  held  breath  may  evoke  a  premature  beat, 
and  the  opportunity  of  detecting  alternation  in  this  manner 
should  not  be  lost. 

Single  premature  beats  are  usually  followed  by  a  pulsa- 
tion of  exceptional  size,  for  the  heart  puts  out  more  than  its 
usual  quantum  of  blood.  It  is  the  pulse  which  succeeds  this 
tail  beat  which  shows  the  first  sign  of  weakening  ;  it  is  less 
forcible  than  that  which  succeeds  it.  In  Fig.  54  a  regular 
pulse  is  interrupted  by  a  single  premature  contraction  (p)  ; 


«i    ii>»urw»tf>.iarvuji>'*''t>'vv 


■VVl'VIO*'*'*"'^ 


Fig.  54.     Alternation  of  the  pulse,  appearing  after,  and  as  a  result  of,  a 
single  premature  beat  ]?.     It  lasts  for  four  heart  cycles. 


it  is  followed  by  the  usual  pause,  and  this  is  succeeded  by  a  tall 
pulsation  (l)  ;  the  next  beat  s^  is  small,  it  is  followed  by  a 
taller  beat  l^.  The  small  beat  s'^  is,  as  I  have  said,  the  earliest 
sign  of  the  condition,  and  it  may  be  the  sole  sign.  In  the 
actual  figure  s^,  the  next  alternate  beat,  is  also  low.  Alterna- 
tion has  proceeded  for  four  cycles  before  the  normal  pulse 
beats  are  restored.  In  Figs.  52  and  53  the  condition  is 
persistent  throughout  each  curve  ;  little  and  big  beats  are 
arranged  alternately.  Extreme  degrees  of  alternation  of  the 
pulse  are  seldom  encountered  ;  but  on  very  rare  occasions 


118  Chapter    VI 11. 

the  little  beats  vanish  entirely,  and  the  pulse  rate  is  halved 
for  short  periods. 

The  other  irregularity  with  which  pulsus  alternans  may 
be  confused  is  a  coupled  pidse  resulting  from  premature 
beats,  but  this  only  happens  when  tlie  prematurity  of  the 
second  beat  of  each  couple  is  slight.  An  example  is  shown 
in  Fig.  33  of  an  earlier  chapter.  There  is  sufficient  contrast 
between  them  ;  whereas  the  little  beat  in  Fig.  33  is  followed 
by  the  longer  pause,  if  pulsus  alternans  is  present  the  little 
beat  is  followed,  if  there  is  any  variation  in  pauses,  ))y  the 
slightlj^  shorter  pause.  \\\  tracings  written  upon  slowly 
travelling  paper  a  difference  in  intervals  is  hardly  perceptible 
(Fig.  52)  ;  but  Avhere  the  paper  has  moved  faster,  a  measure- 
able  difference  is  often  found  ;  it  is  well  seen  in  Fig.  54,  in 
which  the  pauses  following  I  and  l^  are  longer  tlian  those 
followino-  s^  and  6'^. 


The  subjective  sensations  of  patients  presenting  pulsus 
alternans. 

Alternation  of  the  heart  is  responsible  for  no  sj'mptoms  ; 
the  patient  only  complains  of  sensations  wliich  are 
referable  to  other  causes.  Thus,  anginal  pain  is  common. 
Breathlessness  is  even  commoner  ;  it  is  often  nocturnal, 
repeatedly  awakening  the  subject  of  it  after  short  periods 
of  sleep  and  being  accompanied  by  acute  anxiety.  Breathing 
of  the  Chejaie-Stokes  type  is  rarely  noted  by  those  who 
manifest  this  respiratory  abnormality,  but  periodic  dyspnoea 
may  be  remarked  by  the  friends,  especially  by  those  who 
sleep  with  the  patients. 


Alternation  of  the   Heart.  119 

l^he  prognosis. 

Alternation  of  the  pulse  belongs  to  a  small  group  of 
phenomena  witnessed  by  those  who  attend  the  sick,  which, 
treated  as  isolated  signals,  are  in  themselves  emphatic  and 
portentous.  It  ranks  with  subsultus  tendinum,  with  optic 
neuritis,  with  the  risus  sardo7iicus  and  other  ill-omened 
messengers.  It  is  the  faint  cry  of  an  anguished  and  fast 
failing  muscle,  which,  when  it  comes,  all  should  strain  to  hear, 
for  it  is  not  long  repeated.  A  few  months,  a  few  years  at 
most,  and  the  end  comes. 

How  grave  is  the  condition  of  the  patient  whose  heart 
•produces  this  alternating  pulse  is  often  witnesied  to  by 
associated  signs  ;  angina,  nocturnal  dyspnoea,  Cheyne-Stokes 
breathing  or  high  blood  pressure  are  often  encountered  in  the 
same  subject.  But  here  lies  its  special  significance  :  each 
and  all  of  these  signs  may  fail,  while  alternation  is  there 
to  tell  the  future.*     Unexpected  death  is  not  uncommon. 

I  write  of  continued  alternation  of  the  pulse  wMch 
alternates  in  force  for  many  cycles.  It  is  persistent  while 
the  heart  yet  lives.  The  prognostic  value  of  the  lesser  grades 
of  alternation  is  less  certainly  known  ;  but  that  their  vsigni- 
ficance  is  grave,  and  that  they  are  but  too  often  the  fore- 
runners of  the  fully  developed  condition,  should  be  understood. 
A  favourable  prognosis  is  always  forbidden  by  the  latter, 
and  can  be  but  rarely  justified  in  the  presence  of  the  former. 
The  only  propitious  circumstances  are  a  history  of  exceptional 
and  prolonged  strain  in  the  patient  who  show^s  the  sign, 
strain  which  may  be  at  once  and  permanently  avoided,  or 
the  presence  of  acute  intoxication  which  is  vanishing. 


*  It  is  true,  however,  that  alternation  is  never  the  sole  sign  of  disease  ; 
patients  who  exhibit  it  always  manifest  a  poor  tolerance  of  exercise. 


120  Chapter   VIII. 

The  treatment. 

The  management  of  heart  cases,  in  so  far  as  it  is  affected 
by  this  sign  alternation,  may  be  stated  in  a  few  words,  for 
it  should  be  evident.  Alternation  speaks  of  over-taxation  ; 
it  demands  relief.  In  busy  people  it  calls  for  prompt  and 
drastic  curtailment  of  work,  be  it  mental  or  physical  exertion. 
In  the  more  sedentary,  it  is  an  indication  for  prolonging 
the  hours  of  actual  rest,  both  of  body  and  of  mind  ;  the 
condition  of  such  patients  may  undergo  temporary  relief  by 
a  long  period  of  absolute  quiescence.  In  each  case  sources 
of  anxiety  or  emotion  are  to  be  avoided.  The  presence  of 
alternation  forbids  the  administration  of  general  anaesthetics 
in  major  operations,  unless  the  withholdment  of  the  first 
immediately  jeopardises  life,  or  unless  one  or  other  is  neces- 
sitated for  the  rehef  of  intolerable  pain. 


[       121      ] 


INDEX 


Page 

Accentuated  first  sound         '.  . 

30  &  51 

Adams-Stokes'  Syndrome 

34 

Alternation  of  the  heart 

113 

Angina  and 

114 

Associated  conditions 

114 

Definition  of 

113 

Etiology  of 

114 

Example  of 

.   .                     .    .                     .    .                             b 

Heart  rate  and 

114 

In  experiment 

114 

Mechanism  of 

113 

Prognostic  value  of 

.  .          ....          119 

Recognition  of      .  . 

116 

Subjective  sensations         

118 

Treatment  of 

120 

An.?:sthetics  and  disordered  heart  action 

75,   HI   &  120 

Angina 

Alternation  and   .  . 

114 

Auricular  fibrillation  and 

. .    101  (footnote) 

Paroxysmal  tachycardia  and 

65 

A.S-  Vs  interval    .  . 

IS 

Prolongation  of     .  . 

IS  &  25 

Auricular  fibrillation 

89 

Acute 

112 

Associated  conditions 

92 

Auricular  flutter  and 

87 

Definition  of 

89 

Digitcdis  and 

106 

Example  of 

3 

122 


Index. 


Auricular  iibrillation,  conlinucd- 
Heart -block  and   . . 
Heart  rate  and 
Heart  soinuls  in    .  . 
Infarction  in 
Mitral  stenosis  and 
Morbid  anatomy  in 
Nalnre  of 
Paroxysmal 
Prognosis  in 
Becognition  of 
lielation  to  age 
Relation  to  infective  disease 
Relation  to  sex 
Remarks  iijwn  diagnosis 
Rheumatic,  fever  and. 
Strophanthin  and .  . 
Symptomatology  of 
Thrombosis  in 
Treatment  of 

Auricular  flutter 

Associated  conditions 
Auricular  fibrillation  and 
Definition  of 
Digitalis  and. 
Example  of 
Heart-block  and   .  . 
Morbid  anatomy  in 
Nature  of 
Prognosis  in 
Recognition  of 
Relation  to  age,  etc. 
Strophanthin  and .  . 
Symptomatology  nf 
Treatment  of 

Auricular  sounds 


Page 
91  &   107 
o,  94,  99  &  lOf^ 
98,  99  &   104 
103 
92  &  98 
94 
89 
HI 
105- 
94 
91 
92: 
91 
103 
92: 
109 
101 
103 
100 

76 
79 
87 
76 
87 
3^ 
77 
79- 
76 
86 
7& 
79- 
87 
83 
87 

25  &   SO- 


Auricular  waves 
In  arteries 
In  veins 


32 
:30,  51  &83 


AURICULO-VENTRICULAK    node    and    IJUNDLi: 


17    &   24- 


Index. 


123 


Common  types  of  disordick 
Coupled  heats 
Gross  irregularity  of  2nilse 
Halved  pulse  rate 
Mild  irregularity  of  pulse 
Solitary  pidse  intermittences 
■    Trijjle  beating 

Compensatory  pause 

Coupled  beats 

Digitalis 

Alternation  and   .  . 
Auricidar  Jihr illation  and 
Heart-block  and    .  . 
Premature  beats  and 
Sinus  irregularity  induced  by 

Diastolic  murmues  (see  Presystolic  murmur  also)      26,  28,  53,  98  &  104 


Pag  JO 
0 

6 

29, 

49 

&  108 

7 

&  95 

7 

28 

&  49 

.  .  7 

&  95 

6,  20 

,  47 

&  49 

0 

&  49 
43 

0 

29, 

49 

&  108 

114 
106 

23, 

38 

&  107 

46 

&  56 
14 

Dilatation  (relation  to  heart  rate) 
And  irregularity  .  . 

Diphtheria  and  heart-block  .  . 

Disordered  action  of  the  heart 
Age  incidence 
Frequency .  . 
Heart  rate  and 
Persistence 

Dropped  beats 

extrasystoles  (see  premature  contractions). 

Gross  irregularity 

Halved  heart  rate 

Halved  pulse  rate 

Heart-block 

Blood  j^ressure  in 
Complete   .  . 
Definition  of 


69 

92 

22 


18  &  2(i 


7 

..  7& 

27 

7,  27 

& 

49 

17 
33 

21 

& 

30 
17 

124 


Index 


liiAKT-BLOCK,  continued — 

Pack 

Digitalis  a7id 

..    23,   38  &   107 

Diphtheria  and     .  . 

22 

Effect  of  (on  the  circtdation] 

32 

Etiology     .  . 

21 

Example  of 

2 

Fits  in       .  . 

.   34,  35,  3(1.  37   &  38 

Grades  of  .  . 

18-21   &   25-30 

Heart  rate  in 

5,  27,  30  &  35 

Heart  sounds  in 

.  .    25,    28  &    30 

Heredity  and 

21 

Hypertrophy  in    .  . 

33 

Influenza  and 

22 

Mitral  stenosis  and 

25  &  28 

Morbid  anatomy  in 

24 

Nature  of 

17 

Pneumonia  and    .  . 

22 

Prognosis  in 

36 

Recognition  of      .  . 

25 

Relation  to  age 

21 

Relation  to  chronic  degeneratio>i 

23 

Relation  to  infective  disease 

22 

Relatio7i  to  sex 

21 

Rheumatic  fever  and 

22  &  23 

Symptoms  of 

32 

Syphilis  and 

.  .      22-24 

Treatment  of 

38 

2  :  1  heart-block     .  . 

20&  27 

Typhoid  and 

22 

Vagus  and 

24 

Heaet  katk 

Alternation  and   .  . 
Auricular  fibrillation  and 
Auricular  flutter  and 
Dilatation  and 

Fast  

Halved 

Heart-block  and    .  . 
Premature  contractions  and 
Sinus  irregularity  and     .  . 
Slow  


] 

114 

5, 

94, 

99  & 

109 

5,  76  &  80 

69 

;- 

,10 

57   & 

76 

.    7& 

27 

.    .   5 

27 

30  & 

35 

.   5& 

46 

.   5& 

15 

5,   10. 

27 

30  & 

91 

Index, 


125 


Heart  sounds 

Auricular  fibrillation  and 
Auricular  sounds 
•    First  sound  intensified 
First  sound  reduplicated . 
Grouping  of 
Heart-block  and    .  . 
Mitral  stenosis  and 
Paroxysmal  tachycardia  and 
Premature  contractions  and 
Second  sound  reduplicated 

Heart  strain         .  .  . . 

Infarction  and  fibrillation    .  . 


Page 

98,  99  &  104 
25  &  30 
30  &  51 

25 
49 

25,  28  &  30 
26,  28,  02,  98  &  104 
62 
. .47  &  49 
25 

68 
103 


Influenza 

Auricular  fibrillation  and 
Heart-block  in 

Intermittence  of  pulse 

Mitral  stenosis 

Auricular  fibrillation  and 
Heart-block  and    .  . 
Heart  sounds  in 
Paroxysmal  tachycardia  and 

Morbid  anatomy 

Auricular  fibrillation  and  its 
Auricular  flutter  and  its 
Heart-block  and  its  .  .' 

Paroxysmal  tachycardia  and  its 

Pacemaker 

Paroxysmal  tachycardia  (simple  form) 
Angina  and 
Associated  conditions 
Definition  of 
Differential  diagnosis  of 
Factors  promoting  attacks 
Heredity  and 
Mitral  stenosis  and 


92 

22 

,6 

26  & 

92  & 
25  & 

49 

98 
28 

26, 

28, 

62, 

98  & 
60  & 

104 
62 

94 
79 
24 
61 

10 

57 
65 
60 
57 
66 
60 
59 
60  &  62 


126 


Index. 


,*A1U)XVS.MAL    TACHYCAKDIA    (.SIMl'LK    FOKM),    COXtinuecI 

Page 

Morbid  anatomy  of 

61 

Nature  of 

57 

Posture  and 

Q2&  09 

Premature  contractions  and 

58  &  63 

Prognosis  of 

70 

Relation  to  age 

59 

Relation  to  infective  diseases 

, 

60 

Relation  to  sex 

59 

Rheumatic  fever  and 

00 

Symptomatology  of 

04 

Syphilis  and 

00 

Treatment  of 

73 

Phasic  vakiations  of  pulse  rate 


14 


Pneumonia 

Alternation  and  .  . 
Auricular  fibrillation  and 
Heart-hlocl-  and    .  . 

PllEMATUKE    CONTKACTIONS   (EXTEASYSTOLES) 

Associated  conditions 

Auricular. 

Definition  of 

Digitalis  and 

Example  of 

Fatigue  and 

Heart  rate  and 

Heart  sounds  in  .  . 

Nature  of 

Paroxysmal  tachycardia  and 

Posture  and 

Prognosis  of 

Provocative  factors 

Recognition  of 

Relation  to  age  and  sex 

Subjective  phenomena  in 

Tobacco  and 

Treatment  of 

Ventricular 

PrKSYSTOT.IC    MURML'K    (DISAn'KARAXC'E    OF) 


114 

112 

22 

41 

44 

43  & 

40 

41 

46  & 

66 

2 

46 

..    5& 

46 

47  & 

49 

41 

o8  &. 

63 

47 

54 

45 

47 

44 

53 

40 

54 

42  & 

49 

.  .       53,   62  & 

98 

Index. 


127 


Prognosis 

Alternation  of  the  heart  and 
Auricular  fibrillation  and 
Auricular  flutter  and 
Heart-block  and    .  . 
Paroxysmal  tachycardia  and 
Premature  contractions  and 
Sinus  irregularity  and 


-Pulsus  alternans  (see  alternation  of  the  heart) 


J'agk 
119 
105 
86 
36 
70 
54 
15 

113 


Pulse  rate  (see  Heart  rate) 
Halved  jndse  rate 

pubkinje  network 

Reduplicated  first  sound 

,,  second  sound 

JRefractory  state 
JRespiratory  irregularities 


JRheumatic  fever 

Auricular  fibrillation  and 
Auricular  flutter  and 
Heart-block  and    .  . 
Paroxysmal  tachycardia  and 

^INO -AURICULAR   NODE 
mSiNUS    IRREGULARITIES 

Definition  of 

Digitalis  and 

Example  of 

Heart  rate  and 

Nature  of 

Phasic  variation  .  . 

Prognostic  significance  of 

Recognition  of   ,  . 

Relation  to  respiration 

Standstill  of  the  heart 

Tt(berculosis  meningitis  and 


1,  27  &  49 
17 

.  .  25  &  30 

..  25&  30 

43 

12 


92 
79 
22  &  23 
60 


8 
8 
14 
2 
5  &  15 
8 
14 
16 
15 
12  &  15 
14 
16  (footnote) 


128 


Index. 


Slonv  rri,SK  5,     10.  2  L 

Standstill  of  tiil  iii:akt 

Stkophanthin 

Auricular  fibrillation  and 
Anrimlar  flutter  and 

Sympathetic  nkkves 

Syphilis 

Auricular  flutter  and 
Heart-block  and    .  . 
Paroxysmal  tachycardia  and 

Tobacco  and  pulse  irregulaeity 

Treatment 

Alternation  of  the  heart  and 
Auricular  fibrillation  and 
Auricular  flutter  and 
Heart-block  and    .  . 
Paroxysmal  tachycardia  and 
Premature  contractions  and 

Triple  beating 

Tuberculous  meningitis  and  irregular  pulse 

Typhoid  and  heart-block 

Vagus       . .  8,  10,  15, 

Venous  pulsation 


Page 

30,  40  &  91 

14 


109 

87 

8&47 


70 

22-24 

60 

4& 


12a 

106 

87 

38 

75 

54 

.    6&  49- 

LG( 

footnote)- 

22 

24, 

73  &  80 

30, 

51  &  8a 

SHAW  &  SONS,  FHTTEH  LA\E,  LONDON,  E.C.4. 


COLUMBIA  UNIVERSITY  LIBRARIES 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing,  as 
provided  by  the  library  rules  or  by  special  arrangement  with 
the  Librarian  in  charge. 

DATE   BORROWED 

DATE    DUE 

DATE    BORROWED 

DATF     DUE 

C28(842)M50 

